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Chemoresistance in gastric cancer is attributed to the overexpression of excision repair cross‐complementing 1 (ERCC1) caused by microRNA‐122 dysregulation

MicroRNAs are deemed as key regulators of gene expression. In particular, the elevated expression of excision repair cross‐complementing 1 (ERCC1) significantly reduced the effectiveness of gastric cancer treatment by cisplatin (CDDP)‐based therapies. In this paper, qRT‐PCR and western blot were adopted to measure miR‐122 and ERCC1 messenger RNA (mRNA) expression in all samples. Luciferase assay was carried out to verify the role of ERCC1 as a target of miR‐122. The CCK‐8 assay was carried out to study the effect of ERCC1 and miR‐122 on cell survival and apoptosis. The results demonstrated that miR‐122 expression was reduced in cisplatin‐resistant gastric cancer. Using bioinformatic analysis, miR‐122 was shown to target the 3′‐UTR of human ERCC1. A dual‐luciferase assay demonstrated that miR‐122 downregulated ERCC1 expression, while the mutations in ERCC1 3′‐UTR abolished its interaction with miR‐122. Transfection of miR‐122 mimics decreased the levels of ERCC1 mRNA and protein expression, while the transfection of miR‐122 inhibitors increased the levels of both ERCC1 mRNA and protein expression. Furthermore, we found that overexpressed miR‐122 promoted the proliferation of MKN74 cells and reduced their apoptotic by targeting ERCC1. In addition, the levels of miR‐122 and ERCC1 were negatively correlated in gastric cancer samples. In summary, the reduced miR‐122 expression may play an essential role in the induction of cisplatin‐resistance by increasing ERCC1 expression.