PMCID string | Title string | Sentences string |
|---|---|---|
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Transfect 293T cells using Lipofectamine 2000, and replace the medium with fresh medium after 6h. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Check the transfection efficiency using the fluorescence microscope after 48h of transfection, and collect the supernatant after 72h. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The GIST-882 or GIST-T1 cells were added with the corresponding volume of polybrene 0.5h before the addition of virus infection. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The cells were replaced after 12h of infection, after 48h the infection efficiency was observed under a fluorescence microscope. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The bottom of the Trans-well chambers (BD) was evenly spread with substrate gel and placed in an incubator at 37 °C for 0.5h to allow solidification. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | After cell counting, the cells were mixed with serum-free DMEM and added directly to the chambers, and the appropriate volume of complete medium was added outside the chambers. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The cells were fixed with methanol, stained crystal violet, and photographed under a microscope. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The average of five random fields of view per chamber was taken to compare each group's migration and invasion ability. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | In this experiment, 3–5 replicate wells were set up to test various cells. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The viability of cells was measured in vitro using the CCK-8 kit. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | 2 × 10 cells per well were inoculated in a 96-well plate and incubated for 48h. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The 10 % CCK-8 solution was added to each well and incubated for approximately 2h. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The absorbance of each well was measured at 450 nm. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | For cell digestion and counting, the suspension was added to a six-well plate for incubation with 1 × 10 cells per well. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Clones were observed after 9–14 days. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Wash twice with PBS, add 1 ml of methanol to each well for fixation, and leave for 10min at room temperature. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Stain with 0.1 mg/ml crystal violet and leave for 10min at room temperature. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Dry and count at room temperature. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Cell membrane components were isolated from GIST-882 cells of imatinib-resistant strain and tissues of GIST-resistant patients (Beyotime Membrane Extraction Kit and Magna RIP™ RNA-Binding Protein Immunoprecipitation Kit). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Total RNA and cell membrane RNA were extracted with TRIZOL reagent, and PIGR endogenous antibody for RIP-Seq experiments. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Validation was performed using RIP-RT-PCR. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | 3′ RACE and 5′ RACE experiments were performed using kits from SMARTer RACE cDNA Amplification Kit (Clontech). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Northern-blot assays were performed using the Northern Max® Kit from Thermo Fisher Scientific. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The online website STRING (https://cn.string-db.org/) was used to predict proteins with potential interactions with PIGR. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Based on the Coding Potential Calculator (CPC, http://cpc.cbi.pku.edu.cn/), the Coding-Potential Assessment Tool (CPAT, http://cpc.cbi.pku.edu.cn/), and Phylogenetic Codon Substitution Frequencies (PhyloCSF score), the LINC00870 sequence was analyzed for protein-coding ability. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The original data of Sarcoma second-generation sequencing were collected from the TCGA database. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | All statistical analyses of bioinformatics were performed with Rstudio software (version 4.0.2; http://www.rstudio.com/products/rstudio). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The Limma package was used to analyze the differences in gene expression between tumor samples and healthy samples, and a volcano map and heat map were drawn. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | R package clusterProfiler (https://guangchuangyu.github.io/software/clusterProfiler) was used to process the GSEA analysis. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The correlation analysis and visualization of the gene expression result were processed using ggplot2 in R software. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Statistical analyses were performed using GraphPad Prism 9 (GraphPad, San Diego, California). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Statistical analysis was done using the paired Student's t-test, the Pearson correlation, or the Log-rank survival analysis. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The p-values less than 0.05 were considered statistically different. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | In this study, we performed RNA sequencing analysis on five GIST patients (cancer and paracancerous tissues) who were resistant to imatinib therapy. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | We combined these results with RNA sequencing data obtained from 263 TCGA-Sarcoma tumor tissues and two normal tissues. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Using filtering conditions of log2Fold change (Tumor/Normal) > 4 and Pearson correlation coefficient (P < 0.001), we identified three genes (PIGR, AKR7A3, PLS1) that were highly expressed in GIST patients who were resistant to imatinib therapy (Fig. S1 A-C). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The differential gene expression profiles analysis between the two data sets indicated that the PIGR gene was significantly highly expressed in GIST imatinib-resistant patients (Fig. 1A and B). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Further analysis of the signaling pathways closely regulated by PIGR using Gene Set Enrichment Analysis (GSEA) showed that PIGR played an inhibitory role in multiple immune activation pathways, such as immune receptor activation and organ- or tissue-specific immune responses (Fig. 1C). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | We utilized the STRING online prediction tool to identify potential molecular targets of PIGR and examined their correlation at the mRNA level. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Our analysis revealed a significant association between PIGR and VNN1 as well as CEACAM6 (Fig. 1D and E). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Vanin-1 (VNN1) has pantetheinase activity and plays a crucial role in tumorigenesis and immune regulation [, , , , ]. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | CEACAM6, a carcinoembryonic antigen immunoglobulin family member, is a cell surface adhesion factor that plays a vital role in tumorigenesis, proliferation and metastasis . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Based on the results obtained in this study, it is reasonable to infer that PIGR may have a pivotal role in regulating immune responses and promoting tumor progression. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Fig. 1PIGR as a candidate gene for the study.(A–B) Hot-map showed the expression profiles of apparently differential genes. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The analysis of the signaling pathways that regulate PIGR using GSEA. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | D–E) The online website STRING was used to predict proteins with potential interactions with PIGR and these proteins were analyzed for relevance at the mRNA level using bioinformatics. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Fig. 1 PIGR as a candidate gene for the study. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | A–B) Hot-map showed the expression profiles of apparently differential genes. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The analysis of the signaling pathways that regulate PIGR using GSEA. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | D–E) The online website STRING was used to predict proteins with potential interactions with PIGR and these proteins were analyzed for relevance at the mRNA level using bioinformatics. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | In light of the crucial role of PIGR in GIST imatinib resistance, we investigated the expression levels of PIGR in imatinib non-resistant cancer samples and their corresponding paracancerous controls, as well as in imatinib-resistant cancer samples and their paracancerous controls. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The results revealed significantly higher mRNA levels of PIGR in GIST tumor samples compared to their paracancerous controls (Fig. 2A, P < 0.001). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Moreover, the mRNA levels of PIGR were markedly higher in imatinib-resistant GIST samples than in non-resistant samples (Fig. 2A, P < 0.001). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | We further categorized the GIST patients into two groups based on PIGR expression levels and examined the correlation between PIGR expression and overall survival time. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The data showed that patients with high PIGR expression levels had a poorer prognosis (Fig. 2B). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Taken together, these results suggest that PIGR is significantly upregulated in imatinib-resistant GIST patients, and higher PIGR expression levels are associated with poorer prognosis. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Fig. 2Expression and prognosis of PIGR in GIST tissues and imatinib-resistant tissues.(A) The mRNA expression of PIGR in different tissues of GIST. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Using the log-rank test, the figure on the left shows the survival analysis of PIGR expression differences in GIST patients. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The figure on the right shows GIST patients divided into positive and negative groups of PIGR expression by RNA-FISH. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | ∗∗∗P < 0.001.Fig. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | 2 Expression and prognosis of PIGR in GIST tissues and imatinib-resistant tissues. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The mRNA expression of PIGR in different tissues of GIST. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Using the log-rank test, the figure on the left shows the survival analysis of PIGR expression differences in GIST patients. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The figure on the right shows GIST patients divided into positive and negative groups of PIGR expression by RNA-FISH. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | ∗∗∗P < 0.001. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | PIGR plays a crucial role in bridging innate and adaptive immunity, suggesting a potential link between imatinib resistance and immune dysregulation [, , ]. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | To further investigate the specific function of PIGR in GIST, we designed sgRNAs against PIGR sequences and performed endogenous interference using CRISPRdCas9 in GIST-T1 and GIST-882 cell lines, followed by relevant cell function experiments. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Our results showed that interfering with PIGR significantly suppressed cell invasion capability, while overexpression significantly promoted it in vitro (Fig. 3A and B). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Furthermore, in vivo experiments showed that overexpression of PIGR significantly promoted lung colonization and liver metastasis of GIST cells (Fig. 3C and D). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | These findings suggest that PIGR acts as an oncogene that promotes the malignant phenotype of GIST.Fig. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | 3PIGR functions as an oncogene in GIST.(A–B) The effect of interfering or overexpressing PIGR on the migration and invasion ability of GIST-T1 and GIST-882 cells. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | C–D) The effect of PIGR overexpression on the invasive ability of GIST-T1 and GIST-882 cells was analyzed via the tail vein model (C) and GIST in situ model (D). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Mean ± SEM of 3 independent experiments. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | ∗∗∗P < 0.001 versus control. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Fig. 3 PIGR functions as an oncogene in GIST. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | A–B) The effect of interfering or overexpressing PIGR on the migration and invasion ability of GIST-T1 and GIST-882 cells. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | C–D) The effect of PIGR overexpression on the invasive ability of GIST-T1 and GIST-882 cells was analyzed via the tail vein model (C) and GIST in situ model (D). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Mean ± SEM of 3 independent experiments. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | ∗∗∗P < 0.001 versus control. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | To facilitate subsequent investigations, we established an imatinib-resistant cell line, GIST-882 (IR-GIST-882), selected based on the SDHB marker as imatinib-resistant . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Our results confirmed the successful construction of the stable resistant cell line (Figs. S2A and B). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | To investigate the molecular mechanisms underlying the role of PIGR in drug-resistant GIST, we extracted RNA from cell membrane fractions of tissues from drug-resistant patients, as well as from cells of drug-resistant strains, for RIP-seq analysis. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | This analysis aimed to identify RNA molecules specifically bound to PIGR (Fig. 4A). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Our study revealed a specific interaction between PIGR and LINC00870 (Fig. 4B), indicating that PIGR may mediate imatinib resistance in GIST through this interaction. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Fig. 4Exploration of specific mechanisms for PIGR.(A) The RIP-seq workflow. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The RNA molecules interacting with PIGR were verified using RIP-PCR. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The workflow was created with BioRender.com. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Fig. 4 Exploration of specific mechanisms for PIGR. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The RIP-seq workflow. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The RNA molecules interacting with PIGR were verified using RIP-PCR. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The workflow was created with BioRender.com. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | To clarify the transcript sequence information of LINC00870 in GIST cells, we conducted RACE assay and Northern-blot assay, which led us to determine the primary transcript length of 2700bp (Fig. 5A and B). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Furthermore, we isolated nucleus and cytoplasmic RNA using extraction kits and discovered that LINC00870 was predominantly localized in the cytoplasmic region (Fig. 5C). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Using bioinformatics tools such as CPC, CPAT, and phyloCSF sites, we predicted that LINC00870 is a non-coding RNA (Fig. 5D). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | To confirm the non-coding nature of LINC00870, we assessed overexpressing LINC00870 cells at both RNA and protein levels. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Agarose gel electrophoresis confirmed effective RNA expression for both sense and antisense strands of LINC00870 (Fig. 5E). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | However, Western blot analysis revealed no protein expression, indicating that LINC00870 RNA does not encode proteins (Fig. 5F).Fig. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | 5Basic characteristics and biological functions of LINC00870.(A) LINC00870 sequence information and length were analyzed using 3′RACE and 5′RACE experiments. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The uncropped gel image can be found in Supplementary Figure 3. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The number and length of LINC00870 transcripts in GIST cell lines and tissues were determined by a Northern blot assay. |
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