| Summary: | Zhe Song,1 Nan Jia,1 Wei Li,1 Xiao-Yu Zhang2 1Second Department of General Surgery, Cangzhou Central Hospital, Cangzhou, Hebei Province, Mainland China; 2Department of Thyroid and Breast III, Cangzhou Central Hospital, Cangzhou, Hebei Province, Mainland ChinaCorrespondence: Xiao-Yu ZhangDepartment of Thyroid and Breast III, Cangzhou Central Hospital, Cangzhou, Hebei Province, People’s Republic of ChinaEmail zhangxiaoyu9321@163.comBackground: Chemotherapy resistance has long been recognized as a major obstacle to cancer treatment. Therefore, elucidating the underlying mechanisms of chemotherapy resistance is conducive to developing new strategies to improve patients’ response to chemotherapy drugs.Materials and Methods: Real-time quantitative PCR (QPCR) was applied to measure the expression levels of lncRNAs. LINC01572 was down-regulated or up-regulated in GC cells transfected with either LINC01572 shRNA or overexpression vectors. In vitro and in vivo experiments were conducted to investigate the role of LINC01572 in autophagy-related chemotherapy resistance.Results: Compared with the parental cells, drug-resistant GC cells had a higher level of LINC01572. Silencing of LINC01572 inhibited chemotherapy-induced autophagy, while its knockout sensitized GC cells against chemotherapy drugs. As a competitive endogenous RNA of miR-497-5p, LINC01572 weakened the inhibitory effect of miR-497-5p on ATG14, leading to chemically induced autophagy and chemotherapy resistance in GC cells.Conclusion: A new mechanism of GC autophagy-related chemotherapy resistance regulated by lncRNA was explored in this study, providing a new perspective for understanding chemotherapy resistance.Keywords: LINC01572, miR-497-5p, gastric cancer, drug resistance
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