Mardiyyah/TAPT_data_V2_split · Datasets at Hugging Face

PMCID stringclasses 24 values	Title stringclasses 24 values	Sentences stringlengths 2 40.7k
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	A bar graph with four bars, the means of 2−ΔΔCt values of 1.00, 1.03, 1.03, and 1.05 being over each bar, which represents the control group, the 6.25µg/ml Endostar group, the 12.5µg/ml Endostar group, and the 25µg/ml Endostar group, respectively, displays the MHC class I α-heavy chain mRNA levels of three independent experiments after treatment of A549 lung cancer cells with Endostar for 24 h. Figure 6.Upregulation by Endostar on the protein of MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells measured by Western blot assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	After treatment with Endostar for 24 h, the protein of MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells was measured by Western blot assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Error bars indicate the SD.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Asterisks indicate p < .05, significantly different compared with the control; one-way analysis of variance followed by LSD test.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	A bar graph (labeled with “HLA-I in A549 cells”) with four bars, the means of the arbitrary units of 0.86, 0.99 with asterisk, 1.05 with asterisk, and 1.10 with asterisk being over each bar, which represent the control group, the 6.25µg/ml Endostar group, the 12.5µg/ml Endostar group, and the 25µg/ml Endostar group, respectively, displays the MHC class I α-heavy chain protein expression levels of three independent experiments after treatment of A549 lung cancer cells with Endostar for 24 h; a bar graph (labeled with “HLA-I in NCI-H1299 cells”) with four bars, the means of the arbitrary units of 0.71, 1.07 with asterisk, 1.08 with asterisk, and 1.10 with asterisk being over each bar, which represent the control group, the 6.25µg/ml Endostar group, the 12.5µg/ml Endostar group, and the 25µg/ml Endostar group, respectively, displays the MHC class I α-heavy chain protein expression levels of three independent experiments after treatment of NCI-H1299 lung cancer cells with Endostar for 24 h. Corresponding protein bands by Western blot were representatively shown under each bar graphs.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Effects of Endostar on the mRNA of MHC class I α-heavy chain in A549 lung cancer cells measured by RT-qPCR assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	After treatment with Endostar for 24 h, the mRNA of MHC class I α-heavy chain in A549 lung cancer cells was measured by RT-qPCR assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Error bars indicate the SD.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Slight enhancement without statistical significance were found among the groups with Endostar treatment (p > .05); one-way analysis of variance.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Upregulation by Endostar on the protein of MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells measured by Western blot assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	After treatment with Endostar for 24 h, the protein of MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells was measured by Western blot assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Error bars indicate the SD.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Asterisks indicate p < .05, significantly different compared with the control; one-way analysis of variance followed by LSD test.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	HIF-1 gene was transfected into A549 and NCI-H1299 cells to overexpress HIF-1.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	It was shown that the relative levels of β2 m (β light chain) and α heavy chain of MHC-I protein were statistically decreased in HIF-1-over-expressing A549 cells and NCI-H1299 cells compared with the NC control A549 cells and NCI-H1299 cells (p = .019, p = .041, p = .000, and p = .048), respectively (Figure 7 in detail).
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Figure 7.Downregulation by HIF-1 over-expression on β2-microglobulin and MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells measured by Western blot assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	After transfection with over-expressing HIF-1 gen into the cells for 48 h, the proteins of β2-microglobulin and MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells were measured by Western blot assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Error bars indicate the SD.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Asterisks indicate p < .05, significantly different compared with the control; independent-sample t test.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	A bar graph with four bars (the first two bars were labeled with “β2m in A549 cells” and the last two bars were labeled with “β2m in NCI-H1299 cells”), the means of the arbitrary units of 1.12, 0.9 with asterisk, 1.3, and 0.74 with asterisk, being over each bar, which represent the NC transfection group and HIF-1 transfection group of A549 cells, and the NC transfection group and HIF-1 transfection group of NCI-H1299 cells, respectively, displays the β2-microglobulin protein expression levels of three independent experiments after transfection with over-expressing HIF-1 gen or NC gen into the cells for 48 h; a bar graph (the first two bars were labeled with “HLA-I in A549 cells” and the last two bars were labeled with “HLA-I in NCI-H1299 cells”) with four bars, the means of the arbitrary units of 1.11, 0.90 with asterisk, 1.06, and 0.91 with asterisk being over each bar, which represent the NC transfection group and HIF-1 transfection group of A549 cells, and the NC transfection group and HIF-1 transfection group of NCI-H1299 cells, respectively, displays the HLA-I α-heavy chain expression levels of three independent experiments after transfection with over-expressing HIF-1 gen or NC gen into the cells for 48 h. Corresponding protein bands by Western blot were representatively shown under each bar graph.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Downregulation by HIF-1 over-expression on β2-microglobulin and MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells measured by Western blot assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	After transfection with over-expressing HIF-1 gen into the cells for 48 h, the proteins of β2-microglobulin and MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells were measured by Western blot assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Error bars indicate the SD.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Asterisks indicate p < .05, significantly different compared with the control; independent-sample t test.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	MHC class I may be regulated by JAK2/STAT3 signaling pathway.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	It was shown that the relative levels of STAT3 in A549 cells in the groups treated with 6.25 μg/ml, 12.5 μg/ml, and 25 μg/ml Endostar were statistically decreased (p = .004, p = .008, p = .010, respectively) compared with the control group (Figure 8 in detail).
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	STAT3 is activated by phosphorylation.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	After a treatment of A549 lung cancer cells with Endostar for 24 hours, the relative levels of pSTAT3 were statistically decreased with statistical significance in the groups treated with 12.5 μg/ml (p = .037) and 25 μg/ml (p = .003) Endostar compared with the control group (Figure 8 in detail).
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Figure 8.The downregulation of STAT3 and pSTAT3 proteins in A549 lung cancer cells by Endostar measured by Western blot assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	After treatment with endostar for 24 h, the protein of STAT3 and pSTAT3 in A549 lung cancer cells was measured by Western blot assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Error bars indicate the SD.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Asterisks indicate p < .05, significantly different compared with the control; Hashtags indicate p < .05, significantly different compared with the group treated with 6.25 μg/ml Endostar; one-way analysis of variance followed by LSD test.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	A bar graph (labeled with “STAT3 in A549 cells”) with four bars, the means of the arbitrary units of 1.21, 0.92 with asterisk, 0.96 with asterisk, and 0.96 with asterisk being over each bar, which represent the control group, the 6.25µg/ml Endostar group, the 12.5µg/ml Endostar group, and the 25µg/ml Endostar group, respectively, displays the STAT3 protein expression levels of three independent experiments after treatment of A549 lung cancer cells with Endostar for 24 h; a bar graph (labeled with “pSTAT3 in A549 cells”) with four bars, the means of the arbitrary units of 1.28, 1.09, 0.97 with asterisk, and 0.74 with asterisk and hashtags being over each bar, which represent the control group, the 6.25µg/ml Endostar group, the 12.5µg/ml Endostar group, and the 25µg/ml Endostar group, respectively, displays the pSTAT3 protein expression levels of three independent experiments after treatment of A549 lung cancer cells with Endostar for 24 h. Corresponding protein bands by Western blot were representatively shown under each bar graph.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	The downregulation of STAT3 and pSTAT3 proteins in A549 lung cancer cells by Endostar measured by Western blot assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	After treatment with endostar for 24 h, the protein of STAT3 and pSTAT3 in A549 lung cancer cells was measured by Western blot assay.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Error bars indicate the SD.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Asterisks indicate p < .05, significantly different compared with the control; Hashtags indicate p < .05, significantly different compared with the group treated with 6.25 μg/ml Endostar; one-way analysis of variance followed by LSD test.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	The host immune system exerts immunosurveillance to control cancer development.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	By inducing the expression of immunosuppressive factors, however, tumor HIF-1 signaling subdues both the innate and adaptive immune responses, thereby shielding the tumor from immune attacks.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	In addition, insufficient expression of MHC class I on cancer cells is one of the important strategies employed by cancer to evade the immune system.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Therefore, inhibition of HIF-1 and improvement of MHC class I expression on cancer cells is important to induce effective responses of cell-mediated immunity against cancer such as lung cancer for immunotherapies, including PD-1/PD-L1 inhibitor.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	The effect of Endostar in inhibiting HIF-1 and promoting MHC class I expression on cancer cells, such as lung cancer cells, may counteract cancer immune evasion and thereby benefit cancer immunotherapy.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	However, this remains unclear.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	This study was designed to determine the effect of Endostar in inhibiting HIF-1 and promoting MHC class I expression on lung cancer cells.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Endostar was administrated to A549 and NCI-H1299 lung cancer cells and the protein of HIF-1 and MHC class I and their mRNAs was detected by western blot and RT-qPCR.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	The lower HIF-1 and higher MHC class I were found in Endostar treated A549 and NCI-H1299 cells.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	These findings demonstrated inhibtion on HIF-1 and promotion on MHC class I by Endostar, suggesting the potential of Endostar to benefit lung cancer immunotherapy.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Endostar, an N-terminal modified recombinant human endostatin, is a human recombinant endostatin, an attractive anti-angiogenesis protein.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Therefore, Endostar has anti-angiogenesis effects.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Endostar was developed as a specific drug permitted by the State Food and Drug Administration in China in 2005 for its use in NSCLC therapy.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Endostatin is a natural protein, first isolated and extracted from mouse tumors by Judah Folkman, with a wide antitumor spectrum and strong antiangiogenic capacity.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Angiogenesis is a physiological process of forming new blood vessels from existing blood vessels and circulating endothelial precursors.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	It is essential to the occurrence and development of tumors, which grow rapidly and metastasize eventually.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Physiologically, angiogenesis is essential to physiological processes like embryogenesis, tissue growth, and regeneration.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Oncologically, it is also important for cancer cells that grow rapidly and metastasize eventually because angiogenesis supplies oxygen and nutrients which are deficient in cancer cells for their rapid growth and eventual metastasis.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Therefore, anti-angiogenesis is one of the most important cancer therapies.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Endostar as a recombinant human endostatin with nine added amino acids (MGGSHHHHH) to maintain stability and a long half-life has effective antiangiogenic effect.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Besides, it was shown in this study that Endostar inhibited HIF-1 with upregulation of MHC class I expression in A549 and NCI-H1299 lung cancer cells, benefiting cancer cell killing by effectory lymphocytes.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	HIF-1, a heterodimer consisting of a constitutive β-subunit and an oxygen-sensitive α-subunit, is a main transcriptional regulator responsible for metabolic adaptation to alterations in the oxygen environment.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	It involves in many physiological and pathological processes in the body and is closely associated with the pathogenesis of many diseases.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	In solid tumors, uncontrolled proliferation of cancer cells vs disorganized growth of blood vessels results in limited supply of nutrients and oxygen resulting in low oxygen tension; therefore, regions with hypoxic microenvironments are created.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	In these regions, the highly overexpressed HIF-1 is important to drive tumor growing, invasion, and metastasis in different human cancers.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	The association of a poor survival with the high expression of HIF-1α has been indicated by survival analysis in patients with lung cancer, and different SNPs in HIF-1α may have different effects on overall cancer risk in an ethnicity- and type-specific manner.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Reduction of HIF-1α by Simvastatin enhanced Anti-tumor Effects of Bevacizumab in A549 cells.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Targeting ATM/HIF-1α signaling by solanidine induced anti-angiogenesis and anti-cancer effect in lung cancer.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Besides its involvement in various aspects of tumor development, such as tumor growth, invasion, metastasis, and angiogenesis, HIF-1 is also involved in tumor immune evasion which facilitates cancer cells to proliferate and metastasize, and contributes to failure in immunotherapy.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Inhibition of HIF-1 expression in cancer cells contributes to cancer control and induction of effective anti-cancer immunity in cancer immunotherapy.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Endostar has the effect to down-regulate HIF-1.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	It was shown in this study that 25 μg/ml Endostar inhibited HIF-1 expression in A549 and NCI-H1299 lung cancer cells.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	HIF-1 is induced by hypoxia in cancer cells, and in normoxia, it is not usually observed or only basal expression can be observed.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	In this study, experiments showed a high expression of HIF-1 in control and untreated cells.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	However, this did not necessarily mean that the expression of HIF-1 in control and untreated cells was really high because it was detected with the expression in Endostar treated A549 cells and NCI-H1299 cells as the backgroud.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	The expression detected by Western blot and Immunocytochemistry is relative quantification.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	The assays had been optimized for enough sensitivity to detect the reduced expression in Endostar treated A549 cells and NCI-H1299 cells.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	An effective adaptive response can be achieved through a multi-step antigen processing and pathway, namely the cellular antigen processing machinery (APM).
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Antigens must be processed into antigenic peptides by APM.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	These peptides are loaded onto an MHC class I molecule.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	MHC class I molecules are glycoproteins of heterodimers with a polymorphic heavy chain (α-chain) and an invariable β2 microglobulin (β2 m) light chain (β-chain).
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	The α-chain is encoded by the Human Leukocyte Antigen-HLA A, B, and C genes in humans.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	There is a groove in the MHC class I molecules to preferentially bind 8-11mer peptides.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	The antigenic epitope binds to the exposed surface of this groove as a part of the MHC class I complex.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	It is recognized by the TCR on the T cells.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	This study showed that the expression of MHC class I α-heavy chain and β2 m light chain in A549 and NCI-H1299 lung cancer cells was improved by Endostar, which benefited cancer immunotherapy against the lung cancer cells.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	In the context of HIF-1 down-regulation by Endostar, which was shown in this study, to demonstrate the role of HIF-1 on the MHC class I α-heavy chain and β2 m light chain in A549 and NCI-H1299 lung cancer cells, the over-expressing HIF-1 gene was transfected into A549 and NCI-H1299 cells resulting in decrease of relative levels of MHC class I α-heavy chain and β2 m light chain.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	This results were in line with the decrease of HIF-1 by Endostar treatment accompanied with the enhancement of MHC class I α-heavy chain and β2 m light chain.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	In addition to the important role in metabolic adaptation to hypoxia stress caused by deficient supply of nutrients and oxygen because of uncontrolled growth of cancer cells and disorganized neoangiogenesis, the signaling pathways of HIF-1, a heterodimer highly expressed in a variety of tumor cells, suppress innate and adaptive immune systems to escape immune attack.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	That HIF-1 downregulates the antigen presenting MHC class I molecules is an important strategy for cancer to evade immune attack, because only in combination with MHC class I on the target cells, can tumor antigenic peptides be recognized by CD8+ CTL with the subsequent destruction of the target cells.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Theoretically, inhibition of HIF-1 may upregulate the expression of MHC class I on cancer cells.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	This study demonstrated that 25 μg/ml Endostar inhibited expression of HIF-1 with the upregulation of MHC class I α-heavy chain and β2 m light chain in A549 and NCI-H1299 lung cancer cells, suggesting the potential for Endostar to facilitate cancer immunotherapy.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Experimental evidence, however, is required and further research with experimental evidence remains to be performed in the future to confirm the possible suppression of immune evasion tactic with endostar treatment.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Other limitations such as lack of an in vivo tumor model and further validation using flow cytometry remain to be supplementarily performed in the future.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	The mechanism of MHC class I regulation involves the innate immune molecule NLR family CARD domain containing 5 (NLRC5), which is a member of recently discovered NLRs-like receptor family of the highly conserved one.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	NLRC5 is an MHC class I gene transactivation factor which induces the MHC class I gene transcription and subsequently activates antigen presentation process.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	NLRC5 is transcriptionally regulated in JAK2/STAT3 signaling-dependent pathway.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	This study demonstrated that some concentrations of Endostar decreased the relative levels of STAT3 and pSTAT3 in A549 lung cancer cells with statistical significance, which is in line with the role of JAK2/STAT3 pathway in regulation of MHC class I via NLRC5, suggesting the underlying mechanism of MHC class I upregulation involving JAK2/STAT3 signaling pathway.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	Endostar (25 μg/ml) inhibited the expression of HIF-1 with the upregulation of MHC class I α-heavy chain and β2 m light chain in A549 and NCI-H1299 lung cancer cells, which showed the potential for Endostar to facilitate cancer immunotherapy.
PMC12101583	Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.	It is needed for future studies that are warranted to confirm the role of Endostar treatment.
PMC11541409	Current Drug Resistance Mechanisms and Treatment Options in Gastrointestinal Stromal Tumors: Summary and Update.	Gastrointestinal stromal tumor (GIST) is characterized by well-defined oncogenes.
PMC11541409	Current Drug Resistance Mechanisms and Treatment Options in Gastrointestinal Stromal Tumors: Summary and Update.	Despite the significant improvement in treatment outcomes with adjuvant imatinib therapy for patients, drug resistance remains a major challenge for GIST therapy.
PMC11541409	Current Drug Resistance Mechanisms and Treatment Options in Gastrointestinal Stromal Tumors: Summary and Update.	This review focuses on the mechanisms contributing to drug resistance phenotype in GIST, such as primary imatinib-resistant mutants, secondary mutations, non-covalent binding of TKI to its target, tumor heterogeneity, re-activation of pro-survival/proliferation pathways through non-KIT/PDGFRA kinases, and loss of therapeutic targets in wild-type GIST.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

A bar graph with four bars, the means of 2−ΔΔCt values of 1.00, 1.03, 1.03, and 1.05 being over each bar, which represents the control group, the 6.25µg/ml Endostar group, the 12.5µg/ml Endostar group, and the 25µg/ml Endostar group, respectively, displays the MHC class I α-heavy chain mRNA levels of three independent experiments after treatment of A549 lung cancer cells with Endostar for 24 h. Figure 6.Upregulation by Endostar on the protein of MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells measured by Western blot assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

After treatment with Endostar for 24 h, the protein of MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells was measured by Western blot assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Error bars indicate the SD.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Asterisks indicate p < .05, significantly different compared with the control; one-way analysis of variance followed by LSD test.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

A bar graph (labeled with “HLA-I in A549 cells”) with four bars, the means of the arbitrary units of 0.86, 0.99 with asterisk, 1.05 with asterisk, and 1.10 with asterisk being over each bar, which represent the control group, the 6.25µg/ml Endostar group, the 12.5µg/ml Endostar group, and the 25µg/ml Endostar group, respectively, displays the MHC class I α-heavy chain protein expression levels of three independent experiments after treatment of A549 lung cancer cells with Endostar for 24 h; a bar graph (labeled with “HLA-I in NCI-H1299 cells”) with four bars, the means of the arbitrary units of 0.71, 1.07 with asterisk, 1.08 with asterisk, and 1.10 with asterisk being over each bar, which represent the control group, the 6.25µg/ml Endostar group, the 12.5µg/ml Endostar group, and the 25µg/ml Endostar group, respectively, displays the MHC class I α-heavy chain protein expression levels of three independent experiments after treatment of NCI-H1299 lung cancer cells with Endostar for 24 h. Corresponding protein bands by Western blot were representatively shown under each bar graphs.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Effects of Endostar on the mRNA of MHC class I α-heavy chain in A549 lung cancer cells measured by RT-qPCR assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

After treatment with Endostar for 24 h, the mRNA of MHC class I α-heavy chain in A549 lung cancer cells was measured by RT-qPCR assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Error bars indicate the SD.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Slight enhancement without statistical significance were found among the groups with Endostar treatment (p > .05); one-way analysis of variance.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Upregulation by Endostar on the protein of MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells measured by Western blot assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

After treatment with Endostar for 24 h, the protein of MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells was measured by Western blot assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Error bars indicate the SD.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Asterisks indicate p < .05, significantly different compared with the control; one-way analysis of variance followed by LSD test.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

HIF-1 gene was transfected into A549 and NCI-H1299 cells to overexpress HIF-1.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

It was shown that the relative levels of β2 m (β light chain) and α heavy chain of MHC-I protein were statistically decreased in HIF-1-over-expressing A549 cells and NCI-H1299 cells compared with the NC control A549 cells and NCI-H1299 cells (p = .019, p = .041, p = .000, and p = .048), respectively (Figure 7 in detail).

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Figure 7.Downregulation by HIF-1 over-expression on β2-microglobulin and MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells measured by Western blot assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

After transfection with over-expressing HIF-1 gen into the cells for 48 h, the proteins of β2-microglobulin and MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells were measured by Western blot assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Error bars indicate the SD.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Asterisks indicate p < .05, significantly different compared with the control; independent-sample t test.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

A bar graph with four bars (the first two bars were labeled with “β2m in A549 cells” and the last two bars were labeled with “β2m in NCI-H1299 cells”), the means of the arbitrary units of 1.12, 0.9 with asterisk, 1.3, and 0.74 with asterisk, being over each bar, which represent the NC transfection group and HIF-1 transfection group of A549 cells, and the NC transfection group and HIF-1 transfection group of NCI-H1299 cells, respectively, displays the β2-microglobulin protein expression levels of three independent experiments after transfection with over-expressing HIF-1 gen or NC gen into the cells for 48 h; a bar graph (the first two bars were labeled with “HLA-I in A549 cells” and the last two bars were labeled with “HLA-I in NCI-H1299 cells”) with four bars, the means of the arbitrary units of 1.11, 0.90 with asterisk, 1.06, and 0.91 with asterisk being over each bar, which represent the NC transfection group and HIF-1 transfection group of A549 cells, and the NC transfection group and HIF-1 transfection group of NCI-H1299 cells, respectively, displays the HLA-I α-heavy chain expression levels of three independent experiments after transfection with over-expressing HIF-1 gen or NC gen into the cells for 48 h. Corresponding protein bands by Western blot were representatively shown under each bar graph.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Downregulation by HIF-1 over-expression on β2-microglobulin and MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells measured by Western blot assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

After transfection with over-expressing HIF-1 gen into the cells for 48 h, the proteins of β2-microglobulin and MHC class I α-heavy chain in A549 and NCI-H1299 lung cancer cells were measured by Western blot assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Error bars indicate the SD.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Asterisks indicate p < .05, significantly different compared with the control; independent-sample t test.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

MHC class I may be regulated by JAK2/STAT3 signaling pathway.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

It was shown that the relative levels of STAT3 in A549 cells in the groups treated with 6.25 μg/ml, 12.5 μg/ml, and 25 μg/ml Endostar were statistically decreased (p = .004, p = .008, p = .010, respectively) compared with the control group (Figure 8 in detail).

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

STAT3 is activated by phosphorylation.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

After a treatment of A549 lung cancer cells with Endostar for 24 hours, the relative levels of pSTAT3 were statistically decreased with statistical significance in the groups treated with 12.5 μg/ml (p = .037) and 25 μg/ml (p = .003) Endostar compared with the control group (Figure 8 in detail).

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Figure 8.The downregulation of STAT3 and pSTAT3 proteins in A549 lung cancer cells by Endostar measured by Western blot assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

After treatment with endostar for 24 h, the protein of STAT3 and pSTAT3 in A549 lung cancer cells was measured by Western blot assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Error bars indicate the SD.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Asterisks indicate p < .05, significantly different compared with the control; Hashtags indicate p < .05, significantly different compared with the group treated with 6.25 μg/ml Endostar; one-way analysis of variance followed by LSD test.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

A bar graph (labeled with “STAT3 in A549 cells”) with four bars, the means of the arbitrary units of 1.21, 0.92 with asterisk, 0.96 with asterisk, and 0.96 with asterisk being over each bar, which represent the control group, the 6.25µg/ml Endostar group, the 12.5µg/ml Endostar group, and the 25µg/ml Endostar group, respectively, displays the STAT3 protein expression levels of three independent experiments after treatment of A549 lung cancer cells with Endostar for 24 h; a bar graph (labeled with “pSTAT3 in A549 cells”) with four bars, the means of the arbitrary units of 1.28, 1.09, 0.97 with asterisk, and 0.74 with asterisk and hashtags being over each bar, which represent the control group, the 6.25µg/ml Endostar group, the 12.5µg/ml Endostar group, and the 25µg/ml Endostar group, respectively, displays the pSTAT3 protein expression levels of three independent experiments after treatment of A549 lung cancer cells with Endostar for 24 h. Corresponding protein bands by Western blot were representatively shown under each bar graph.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

The downregulation of STAT3 and pSTAT3 proteins in A549 lung cancer cells by Endostar measured by Western blot assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

After treatment with endostar for 24 h, the protein of STAT3 and pSTAT3 in A549 lung cancer cells was measured by Western blot assay.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Error bars indicate the SD.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Asterisks indicate p < .05, significantly different compared with the control; Hashtags indicate p < .05, significantly different compared with the group treated with 6.25 μg/ml Endostar; one-way analysis of variance followed by LSD test.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

The host immune system exerts immunosurveillance to control cancer development.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

By inducing the expression of immunosuppressive factors, however, tumor HIF-1 signaling subdues both the innate and adaptive immune responses, thereby shielding the tumor from immune attacks.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

In addition, insufficient expression of MHC class I on cancer cells is one of the important strategies employed by cancer to evade the immune system.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Therefore, inhibition of HIF-1 and improvement of MHC class I expression on cancer cells is important to induce effective responses of cell-mediated immunity against cancer such as lung cancer for immunotherapies, including PD-1/PD-L1 inhibitor.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

The effect of Endostar in inhibiting HIF-1 and promoting MHC class I expression on cancer cells, such as lung cancer cells, may counteract cancer immune evasion and thereby benefit cancer immunotherapy.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

However, this remains unclear.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

This study was designed to determine the effect of Endostar in inhibiting HIF-1 and promoting MHC class I expression on lung cancer cells.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Endostar was administrated to A549 and NCI-H1299 lung cancer cells and the protein of HIF-1 and MHC class I and their mRNAs was detected by western blot and RT-qPCR.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

The lower HIF-1 and higher MHC class I were found in Endostar treated A549 and NCI-H1299 cells.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

These findings demonstrated inhibtion on HIF-1 and promotion on MHC class I by Endostar, suggesting the potential of Endostar to benefit lung cancer immunotherapy.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Endostar, an N-terminal modified recombinant human endostatin, is a human recombinant endostatin, an attractive anti-angiogenesis protein.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Therefore, Endostar has anti-angiogenesis effects.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Endostar was developed as a specific drug permitted by the State Food and Drug Administration in China in 2005 for its use in NSCLC therapy.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Endostatin is a natural protein, first isolated and extracted from mouse tumors by Judah Folkman, with a wide antitumor spectrum and strong antiangiogenic capacity.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Angiogenesis is a physiological process of forming new blood vessels from existing blood vessels and circulating endothelial precursors.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

It is essential to the occurrence and development of tumors, which grow rapidly and metastasize eventually.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Physiologically, angiogenesis is essential to physiological processes like embryogenesis, tissue growth, and regeneration.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Oncologically, it is also important for cancer cells that grow rapidly and metastasize eventually because angiogenesis supplies oxygen and nutrients which are deficient in cancer cells for their rapid growth and eventual metastasis.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Therefore, anti-angiogenesis is one of the most important cancer therapies.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Endostar as a recombinant human endostatin with nine added amino acids (MGGSHHHHH) to maintain stability and a long half-life has effective antiangiogenic effect.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Besides, it was shown in this study that Endostar inhibited HIF-1 with upregulation of MHC class I expression in A549 and NCI-H1299 lung cancer cells, benefiting cancer cell killing by effectory lymphocytes.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

HIF-1, a heterodimer consisting of a constitutive β-subunit and an oxygen-sensitive α-subunit, is a main transcriptional regulator responsible for metabolic adaptation to alterations in the oxygen environment.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

It involves in many physiological and pathological processes in the body and is closely associated with the pathogenesis of many diseases.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

In solid tumors, uncontrolled proliferation of cancer cells vs disorganized growth of blood vessels results in limited supply of nutrients and oxygen resulting in low oxygen tension; therefore, regions with hypoxic microenvironments are created.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

In these regions, the highly overexpressed HIF-1 is important to drive tumor growing, invasion, and metastasis in different human cancers.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

The association of a poor survival with the high expression of HIF-1α has been indicated by survival analysis in patients with lung cancer, and different SNPs in HIF-1α may have different effects on overall cancer risk in an ethnicity- and type-specific manner.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Reduction of HIF-1α by Simvastatin enhanced Anti-tumor Effects of Bevacizumab in A549 cells.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Targeting ATM/HIF-1α signaling by solanidine induced anti-angiogenesis and anti-cancer effect in lung cancer.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Besides its involvement in various aspects of tumor development, such as tumor growth, invasion, metastasis, and angiogenesis, HIF-1 is also involved in tumor immune evasion which facilitates cancer cells to proliferate and metastasize, and contributes to failure in immunotherapy.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Inhibition of HIF-1 expression in cancer cells contributes to cancer control and induction of effective anti-cancer immunity in cancer immunotherapy.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Endostar has the effect to down-regulate HIF-1.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

It was shown in this study that 25 μg/ml Endostar inhibited HIF-1 expression in A549 and NCI-H1299 lung cancer cells.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

HIF-1 is induced by hypoxia in cancer cells, and in normoxia, it is not usually observed or only basal expression can be observed.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

In this study, experiments showed a high expression of HIF-1 in control and untreated cells.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

However, this did not necessarily mean that the expression of HIF-1 in control and untreated cells was really high because it was detected with the expression in Endostar treated A549 cells and NCI-H1299 cells as the backgroud.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

The expression detected by Western blot and Immunocytochemistry is relative quantification.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

The assays had been optimized for enough sensitivity to detect the reduced expression in Endostar treated A549 cells and NCI-H1299 cells.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

An effective adaptive response can be achieved through a multi-step antigen processing and pathway, namely the cellular antigen processing machinery (APM).

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Antigens must be processed into antigenic peptides by APM.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

These peptides are loaded onto an MHC class I molecule.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

MHC class I molecules are glycoproteins of heterodimers with a polymorphic heavy chain (α-chain) and an invariable β2 microglobulin (β2 m) light chain (β-chain).

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

The α-chain is encoded by the Human Leukocyte Antigen-HLA A, B, and C genes in humans.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

There is a groove in the MHC class I molecules to preferentially bind 8-11mer peptides.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

The antigenic epitope binds to the exposed surface of this groove as a part of the MHC class I complex.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

It is recognized by the TCR on the T cells.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

This study showed that the expression of MHC class I α-heavy chain and β2 m light chain in A549 and NCI-H1299 lung cancer cells was improved by Endostar, which benefited cancer immunotherapy against the lung cancer cells.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

In the context of HIF-1 down-regulation by Endostar, which was shown in this study, to demonstrate the role of HIF-1 on the MHC class I α-heavy chain and β2 m light chain in A549 and NCI-H1299 lung cancer cells, the over-expressing HIF-1 gene was transfected into A549 and NCI-H1299 cells resulting in decrease of relative levels of MHC class I α-heavy chain and β2 m light chain.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

This results were in line with the decrease of HIF-1 by Endostar treatment accompanied with the enhancement of MHC class I α-heavy chain and β2 m light chain.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

In addition to the important role in metabolic adaptation to hypoxia stress caused by deficient supply of nutrients and oxygen because of uncontrolled growth of cancer cells and disorganized neoangiogenesis, the signaling pathways of HIF-1, a heterodimer highly expressed in a variety of tumor cells, suppress innate and adaptive immune systems to escape immune attack.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

That HIF-1 downregulates the antigen presenting MHC class I molecules is an important strategy for cancer to evade immune attack, because only in combination with MHC class I on the target cells, can tumor antigenic peptides be recognized by CD8+ CTL with the subsequent destruction of the target cells.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Theoretically, inhibition of HIF-1 may upregulate the expression of MHC class I on cancer cells.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

This study demonstrated that 25 μg/ml Endostar inhibited expression of HIF-1 with the upregulation of MHC class I α-heavy chain and β2 m light chain in A549 and NCI-H1299 lung cancer cells, suggesting the potential for Endostar to facilitate cancer immunotherapy.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Experimental evidence, however, is required and further research with experimental evidence remains to be performed in the future to confirm the possible suppression of immune evasion tactic with endostar treatment.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Other limitations such as lack of an in vivo tumor model and further validation using flow cytometry remain to be supplementarily performed in the future.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

The mechanism of MHC class I regulation involves the innate immune molecule NLR family CARD domain containing 5 (NLRC5), which is a member of recently discovered NLRs-like receptor family of the highly conserved one.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

NLRC5 is an MHC class I gene transactivation factor which induces the MHC class I gene transcription and subsequently activates antigen presentation process.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

NLRC5 is transcriptionally regulated in JAK2/STAT3 signaling-dependent pathway.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

This study demonstrated that some concentrations of Endostar decreased the relative levels of STAT3 and pSTAT3 in A549 lung cancer cells with statistical significance, which is in line with the role of JAK2/STAT3 pathway in regulation of MHC class I via NLRC5, suggesting the underlying mechanism of MHC class I upregulation involving JAK2/STAT3 signaling pathway.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

Endostar (25 μg/ml) inhibited the expression of HIF-1 with the upregulation of MHC class I α-heavy chain and β2 m light chain in A549 and NCI-H1299 lung cancer cells, which showed the potential for Endostar to facilitate cancer immunotherapy.

PMC12101583

Inhibitory effect of Endostar on HIF-1 with upregulation of MHC-I in lung cancer cells.

It is needed for future studies that are warranted to confirm the role of Endostar treatment.

PMC11541409

Current Drug Resistance Mechanisms and Treatment Options in Gastrointestinal Stromal Tumors: Summary and Update.

Gastrointestinal stromal tumor (GIST) is characterized by well-defined oncogenes.

PMC11541409

Current Drug Resistance Mechanisms and Treatment Options in Gastrointestinal Stromal Tumors: Summary and Update.

Despite the significant improvement in treatment outcomes with adjuvant imatinib therapy for patients, drug resistance remains a major challenge for GIST therapy.

PMC11541409

Current Drug Resistance Mechanisms and Treatment Options in Gastrointestinal Stromal Tumors: Summary and Update.

This review focuses on the mechanisms contributing to drug resistance phenotype in GIST, such as primary imatinib-resistant mutants, secondary mutations, non-covalent binding of TKI to its target, tumor heterogeneity, re-activation of pro-survival/proliferation pathways through non-KIT/PDGFRA kinases, and loss of therapeutic targets in wild-type GIST.