miR-106a confers cisplatin resistance by regulating PTEN/Akt pathway in gastric cancer cells

Abstract

Recent studies have shown that microRNA-106a (miR-106a) is overexpressed in gastric cancer and contributes to tumor growth. In this study, we investigated whether miR-106a mediated resistance of the gastric cancer cell line SGC7901 to the chemotherapeutic agent cisplatin (DDP). MiR-106a expression was up-regulated in the DDP resistant cell line SGC7901/DDP compared with its parental line SGC7901. Transfection of miR-106a induced DDP resistance in SGC7901, while suppression of miR-106a in SGC7901/DDP led to enhanced DDP cytotoxicity. Further study indicated that the mechanism of miR-106a-induced DDP resistance involved the expression of phosphatase and tensin homolog deleted from chromosome 10 (PTEN) protein and its downstream phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) pathway. This study provides a novel mechanism of DDP resistance in gastric cancer.