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Background/aims: This study aimed to explore the effect of circular RNA ARHGAP26 (circ-ARHGAP26) on cell proliferation and apoptosis in gastric cancer (GC) cell lines., Materials and Methods: Human GC cell lines including HGC-27, AGS, SGC-7901, BGC-823, NCI-N87 and human normal gastric mucosal cells GSE-1 were cultured. The circ-ARHGAP26 expression was determined by quantitative polymerase chain reaction assay. Blank inhibitor and circ-ARHGAP26 inhibitor plasmids were transfected into HGC-27 or AGS cells as NC (-) and circ-ARHGAP26(-) groups. Counting Kit-8 (CCK-8) and Annexin V (AV)/propidium iodide (PI) were conducted to evaluate cell proliferation and cell apoptosis, respectively. Western blot was performed to determine the expressions of apoptotic markers (C-Caspase3 and Bcl-2)., Results: The circ-ARHGAP26 expression was elevated in HGC-27 (P < 0.001), AGS (P < 0.001), SGC-7901 (P < 0.01), BGC-823 (P < 0.05) and NCI-N87 (P < 0.05) GC cell lines compared to GSE-1 cells. In HGC-27 cells, CCK8 assay revealed that cell proliferation was decreased at 48 h (P < 0.05) and 72 h (P < 0.01), while AV/PI assay disclosed that cell apoptosis rate was increased at 72 h in circ-ARHGAP26 (-) group compared to NC (-) group (P < 0.01). Western blot assay also illuminated that apoptotic marker C-Caspase 3 was raised, while anti-apoptotic marker Bcl-2 was reduced at 72 h in circ-ARHGAP26 (-) group compared to NC (-) group. In addition, further validation in AGS cells also exhibited that cells proliferation was repressed, while apoptosis was enhanced in circ-ARHGAP26 (-) group compared to NC (-) group., Conclusion: The circ-ARHGAP26 is over-expressed and its downregulation inhibits cell proliferation and promotes cells apoptosis in GC cells., Competing Interests: None

Background and Objective: The excision repair cross-complementing gene 1 (ERCC1), which is important in the repair of cisplatin-DNA adducts, was reported to be related to cisplatin resistance in tumor cells. The aim of this study is to investigate the changes of cisplatin sensitivity by silencing ERCC1 gene in lung cancer cell., Methods: The small interfering RNA (siRNA) targeting ERCC1 gene was designed and synthesized, and transfected to lung cancer cell A549/DDP. The mRNA and protein expression levels of ERCC1 were evaluated by RT-PCR and Western blot. The changes of cisplatin sensitivity after RNA interference were examined by methyl thiazolyl assay., Results: In A549/DDP cell, the mRNA and protein levels of ERCC1 were decreased and the sensitivity to cisplatin was increased from 12.49 μg/mL to 9.27 μg/mL after transfection., Conclusions: The sensitivity to cisplatin of lung cancer cell A549/DDP could be enhanced by RNA interfering ERCC1 gene targeted code 346.