In conclusion, overexpression of miR-200c-3p may reverse drug resistance in the SGC7901/DDPGC cell line via downregulation of ERCC3 and ERCC4, which suggested this may be part of a mechanism involving the NER pathway.
In the present study, the expression and regulatory mechanisms of miR‑138‑5p were investigated in the gastric cancer cell line SGC7901 and its cisplatin‑resistant derivative SGC7901/DDP.
To investigate the reversing effects of NOTCH1 inhibitor LY3039478 on cancer of the stomach's drug-resistance cells SGC7901/DDP and its relevant mechanism.
Protein and mRNA expression of MerTK were evaluated, and other various <i>in vitro</i> analyses including shRNA transfection, cell cycle anslysis, MTS assay and colony forming assay were carried out with GC cell lines and GC patient-derived cells (PDCs).
Furthermore, the role of the targets neuroblastoma RAS viral (v-ras) oncogene homolog (NRAS) and E2F2 on sensitivity of chemotherapy in GC by MTS and apoptotic cell analysis was assessed.
Our findings revealed the roles of miR-223/FBXW7 signaling in the DDP resistance of GC cells and targeting it will be a potential strategic approach for reversing the DDP resistance in human GC.
With miR-34a mimic and miR-34a inhibitor transfected into SGC-7901 and SGC-7901/DDP for 48 h, post-transfection changes of miR-34a expression was determined; the effects of miR-34a ectopic expression on the viability of cisplatin-induce gastric cancer cell were assayed by the MTT method.