| HRA005411
(Open Access)
|
Imatinib is the preferred targeted therapy for treating gastrointestinal stromal tumor (GIST), but resistance often occurs during treatment, thus limiting its efficacy and clinical application. We performed high-throughput sequencing of tissue specimens from imatinib-resistant GIST patients, screened for polymeric immunoglobulin receptor (PIGR), and identified significantly high expression of PIGR in imatinib-resistant cell lines. We further found that PIGR could specifically bind to LINC00870 and TMEM237, and overexpression of LINC00870 in GIST significantly inhibited the glycosylation modification and secretion of the extracellular region of PIGR, causing immune dysregulation. In this study, after screening PIGR by high-throughput sequencing, we further explored the critical molecules of PIGR in regulating GIST imatinib resistance, and elucidated the mechanism of PIGR in GIST imatinib treatment resistance, to provide a new theoretical basis for blocking drug resistance and improving prognosis. |
