Drug resistance is a key factor affecting the treatment of gastric cancer. The resistance of gastric cancer cells to anticancer drugs, such as cisplatin (DDP), remains a major challenge to patient recovery. The present study aimed to investigate the roles of C-terminal-binding protein 1 (CTBP1) in the DDP resistance of gastric cancer cells and to determine its regulatory effect on DNA repair protein RAD51 homolog 1 (RAD51). The DDP-resistant human gastric cancer AGS and HGC cell lines, AGS/DDP and HGC-27/DDP, respectively, were established and CTBP1 expression was detected by western blotting. In addition, Cell Counting Kit-8, colony formation and flow cytometry assays were performed to detect the proliferation and apoptosis of these two cell lines following CTBP1 knockdown. The expression levels of apoptosis-related proteins were detected by western blotting. In addition, RAD51 was overexpressed in CTBP1 knockdown cells, and proliferation and apoptosis were subsequently determined using the aforementioned methods. The results demonstrated that CTBP1 expression was notably increased in DDP-resistant gastric cancer cells. Furthermore, CTBP1 knockdown suppressed the proliferation and induced the apoptosis of AGS/DDP and HGC-27/DDP cells. Notably, CTBP1 promoted RAD51 expression in DDP-resistant gastric cancer cells. Overexpression of RAD51 in CTBP1 knockdown AGS/DDP and HGC-27/DDP cells rescued the proliferation and alleviated the apoptosis of these cells. Taken together, the results of the present study suggested that CTBP1 may enhance the DDP resistance of gastric cancer cells by activating RAD51 expression, thus providing a potential novel therapy (CTBP1 knockdown) for the clinical treatment of patients with gastric cancer.

Circular RNAs (circRNAs) have been reported to play an important role in the progression of numerous types of human cancer. The aim of the present study was to determine the effects of circRNA_0074027 (circ_0074027) in gastric cancer (GC), and to elucidate the underlying mechanisms of action. For this purpose, the expression of circ_0074027 in GC cell lines was detected using reverse transcription-quantitative PCR. The effects of circ_0074027 on the proliferation and migration of GC cells were investigated using Cell Counting Kit-8 (CCK-8) and Transwell assays, respectively. The Circular RNA Interactome was used to predict that eukaryotic translation initiation factor 4A3 (EIF4A3) could bind to circ_0074027, which was confirmed using an RNA immunoprecipitation assay. The expression and function of EIF4A3 in GC cells were also determined using western blot analysis, as well as CCK-8, colony formation, wound-healing and Transwell assays. The results revealed that circ_0074027 was highly expressed in GC cell lines in the form of a closed loop. In addition, circ_0074027-knockdown inhibited cellular proliferation and motility. Furthermore, EIF4A3 was predicted to be targeted by circ_0074027 and a positive association was identified between them. The overexpression of EIF4A3 reversed the effects of circ_0074027 on the proliferation and motility of GC cells. In conclusion, the findings of the present study demonstrated that circ_0074027 bound to EIF4A3 and promoted the proliferation and migration capacities of GC cells.