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.
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.
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.
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).
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.