PMCID string | Title string | Sentences string |
|---|---|---|
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The uncropped Northern blot image can be found in Supplementary Figure 4. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The distribution of LINC00870 in GIST cell lines. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The sequence protein-coding ability of LINC00870 was predicted using the prediction website. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Agarose gel electrophoresis was utilized to determine the length of LINC00870 in GIST-882 cells overexpressing either the sense or antisense strands. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The uncropped gel image can be found in Supplementary Figure 5. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Western blot analysis was performed to evaluate the protein-coding potential of LINC00870 in GIST-882 cells overexpressing either the sense or antisense strands, with a luciferase plasmid used as the control. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The uncropped Western blot image can be found in Supplementary Figure 6. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The identification of LINC00870 interference and overexpression efficiency. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | H–I) The effect of interfering (H) or overexpressing (I) LINC00870 on GIST cells' invasive and migratory capacity. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | J–K) The effect of interfering (J) or overexpressing (K) LINC00870 on the ability of GIST clone formation. |
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. 5 Basic characteristics and biological functions of LINC00870. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | 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. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The uncropped Northern blot image can be found in Supplementary Figure 4. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The distribution of LINC00870 in GIST cell lines. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The sequence protein-coding ability of LINC00870 was predicted using the prediction website. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Agarose gel electrophoresis was utilized to determine the length of LINC00870 in GIST-882 cells overexpressing either the sense or antisense strands. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The uncropped gel image can be found in Supplementary Figure 5. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Western blot analysis was performed to evaluate the protein-coding potential of LINC00870 in GIST-882 cells overexpressing either the sense or antisense strands, with a luciferase plasmid used as the control. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The uncropped Western blot image can be found in Supplementary Figure 6. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The identification of LINC00870 interference and overexpression efficiency. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | H–I) The effect of interfering (H) or overexpressing (I) LINC00870 on GIST cells' invasive and migratory capacity. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | J–K) The effect of interfering (J) or overexpressing (K) LINC00870 on the ability of GIST clone formation. |
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 | Since lncRNA has been shown to play a crucial role in tumorigenesis and progression [, , , ], we constructed LINC00870 knockdown and overexpression stable cell lines in GIST-T1 and GIST-882 cells to explore its function (Fig. 5G). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | We observed a reduction in cell invasion, migration, and clone formation after LINC00870 knockdown, and an enhancement of these cellular processes after LINC00870 overexpression (Fig. 5H–K). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | These results suggest that LINC00870 functions as an oncogene in GIST. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | We selected two independent cohorts to explore the correlation between PIGR and LINC00870 in GIST imatinib-resistant patient samples to validate our findings. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | We found a significant positive correlation between PIGR and LINC00870 in two cohorts (Fig. 6A, P < 0.0001). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Previous studies have shown that PIGR is a transmembrane glycoprotein whose N-terminal glycosylation promotes hydrolysis and secretion in the extracellular compartment, a critical step in the cellular response to the immune response . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | We investigated the effect of LINC00870 on PIGR by overexpressing it in GIST cells and found a significant decrease in the secretory component content released extracellularly by PIGR (Fig. 6B). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | This result was consistent with the effect of tunicamycin treatment, which disrupts the extracellular glycan chain of PIGR (Fig. 6C). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Our findings suggest that LINC00870 may cause imatinib treatment resistance in GIST by inhibiting the N-terminal glycosylation of PIGR, preventing its extracellular SC region from being released typically and thereby hindering the immune response. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Fig. 6Correlation and mechanism study of PIGR and LINC0087.(A) The correlation analysis between PIGR and LINC00870 at the mRNA level in GIST imatinib-resistant patients. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The unadjusted original results can be found in Supplementary Figure 7. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The expression content of PIGR extracellular secretory structure SC in cell supernatants after overexpression of LINC00870. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The expression content of PIGR extracellular secretory structure SC in cell supernatants after treatment of cells with tunicamycin. |
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. 6 Correlation and mechanism study of PIGR and LINC0087. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The correlation analysis between PIGR and LINC00870 at the mRNA level in GIST imatinib-resistant patients. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The unadjusted original results can be found in Supplementary Figure 7. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The expression content of PIGR extracellular secretory structure SC in cell supernatants after overexpression of LINC00870. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The expression content of PIGR extracellular secretory structure SC in cell supernatants after treatment of cells with tunicamycin. |
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 | In our final analysis, we demonstrated that inhibition of PIGR or LINC0087 effectively overcomes imatinib resistance. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Subcutaneous tumor models were established in BALB/c-nu nude mice using GIST-882 or GIST-882_PIGR_KO resistant cells. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Our results indicate that knockout of PIGR in resistant cell lines effectively inhibits tumor growth (Fig. 7A and B). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Similarly, knockout of LINC0087 in resistant cells also significantly suppresses tumor growth (Fig. 7C and D). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | These findings collectively suggest that inhibition of PIGR or LINC0087 represents a promising strategy for overcoming imatinib resistance. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Fig. 7Inhibition of PIGR or LINC0087 effectively overcomes imatinib resistance.(A–B) Subcutaneous tumor models were established in BALB/c-nu nude mice using GIST-882 or GIST-882_PIGR_KO resistant cells, and tumor growth was monitored (A). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Tumor weight was measured at the end of the experiment (B). ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | C–D) Subcutaneous tumor models were established in BALB/c-nu nude mice using GIST-882 or GIST-882_LINC0087_KO resistant cells, and tumor growth was monitored (C). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Tumor weight was measured at the end of the experiment (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. 7 Inhibition of PIGR or LINC0087 effectively overcomes imatinib resistance. ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | A–B) Subcutaneous tumor models were established in BALB/c-nu nude mice using GIST-882 or GIST-882_PIGR_KO resistant cells, and tumor growth was monitored (A). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Tumor weight was measured at the end of the experiment (B). ( |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | C–D) Subcutaneous tumor models were established in BALB/c-nu nude mice using GIST-882 or GIST-882_LINC0087_KO resistant cells, and tumor growth was monitored (C). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Tumor weight was measured at the end of the experiment (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 | GIST is the most common type of gastrointestinal mesenchymal tumors. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Their pathogenesis is primarily driven by gain-of-function mutations in the KIT gene (accounting for 75–80 %) and mutations in the platelet-derived growth factor receptor alpha (PDGFRA) (<10 %). |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Additionally, abnormalities in genes such as SDH, NF1, KRAS, and HRAS have been implicated in GIST development. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | GIST cells originate from interstitial cells of Cajal or their precursor cells and their survival is dependent on the expression of KIT . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | KIT mutations predominantly occur in the juxtamembrane (JM) domain (encoded by exon 11) and in the extracellular domain near the membrane (encoded by exons 8 or 9), with approximately 85–90 % of KIT-mutant GIST exhibiting these characteristics. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | These mutations confer oncogenic properties to the KIT gene, promoting tumor formation primarily through the PI3K-AKT, JAK-STAT, and RAS-RAF-MEK-ERK (MAPK) signaling pathways [, , , , ]. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Currently, imatinib remains the first-line targeted therapy for progressive or unresectable GIST. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Nevertheless, both primary and secondary drug resistance frequently arise, leading to diminished therapeutic efficacy, increased tumor recurrence, metastasis, and elevated mortality rates. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Thus, elucidating the molecular mechanisms underlying drug resistance in GIST is essential for enhancing therapeutic strategies and prognostic outcomes. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Approximately 90 % of GIST cases are driven by activating mutations in receptor tyrosine kinases, primarily KIT or PDGFRA . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Research on imatinib resistance has highlighted several key factors: KIT mutations result in sustained protein activation, which impacts the genomic context and activates alternative signaling pathways . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Patients with the PDGFRA-D842V mutation exhibit primary resistance to imatinib . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | For BRAF/KRAS mutations, while imatinib inhibits the mutated KIT receptor, it does not affect the downstream RAS-RAF signaling pathways associated with BRAF/KRAS mutations . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Additionally, inhibiting KIT signaling can lead to the release of FGF-2, further worsening tumor malignancy . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | In terms of metabolism, succinate dehydrogenase (SDH) deficiency results in the stabilization and accumulation of HIF1-α under normoxic conditions, promoting angiogenesis and glycolysis, thereby facilitating tumor growth . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Given the extremely limited treatment options for imatinib resistance, there is an urgent need to investigate new mechanisms to combat this challenge. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Our high-throughput sequencing of tissue specimens from imatinib-resistant GIST patients identified PIGR as a significantly differentially expressed gene. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | While PIGR has been found to exhibit differential expression in various cancers, there is no conclusive evidence regarding its role in the prognosis of tumor patients [, , , , , , , ]. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Our study discovered that PIGR is remarkably highly expressed in GIST tumor tissues. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | The role of PIGR in tumors remains controversial, possibly owing to tumor heterogeneity or different action mechanisms. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Studies in colorectal cancer revealed that PIGR could act as a prognostic marker and inhibit tumorigenesis through LAMB3-AKT-FOXO3/4 signaling . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Transcriptome sequencing analysis revealed that PIGR was downregulated in breast cancer, and overexpression of PIGR in breast cancer cells inhibited their adhesion and proliferation . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | PIGR controlled tumor progression in lung cancer by downregulating the differentiation suppressor gene NOTCH3 . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | In hepatocellular carcinoma, extracellular vesicles carrying PIGR activated the AKT/GSK3β/β-linked protein signaling cascade response, promoting cancer stemness, tumorigenesis, and metastasis . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Other studies have revealed that PIGR promoted hepatocellular carcinoma by activating Smad and Yes-MEK/ERK signaling pathways . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Ohkuma et al. found that PIGR overexpression was associated with poor prognosis after surgical resection in patients with pancreatic cancer . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Our study found that GIST patients with high PIGR expression had a poor prognosis, and overexpression of PIGR significantly promoted GIST cell invasion, lung colonization, and liver metastasis, suggesting that PIGR functions as an oncogene in GIST. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Our animal experiments also confirmed that interfering with PIGR expression in imatinib-resistant cell lines helps inhibit tumor growth, suggesting that the application of PIGR inhibitors in clinical settings may improve survival in imatinib-resistant patients. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | However, PIGR plays a critical role in mediating the transcytosis of polymeric IgA and IgM from the basolateral surface to the apical surface of epithelial cells, subsequently secreting these immunoglobulins into the mucosal fluid [, , ]. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Therefore, the sole use of PIGR inhibitors could potentially disrupt normal mucosal immunity. |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | If it is possible to specifically interfere with PIGR at tumor sites, for example, through the use of antibody-drug conjugates (ADCs), it may achieve better therapeutic outcomes while reducing side effects for patients . |
PMC11834037 | LINC00870 promotes imatinib resistance in gastrointestinal stromal tumor via inhibiting PIGR glycosylation modifications | Of course, these conclusions are based solely on animal models, and further challenges must be addressed before clinical application. |
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