Open AccessmiR-106a confers cisplatin resistance by regulating PTEN/Akt pathway in gastric cancer cells
Author(s) -
Yue Fang,
Huiling Shen,
Hao Li,
Yuan Cao,
Rong Qin,
Lingliang Long,
Xiaolan Zhu,
Changqing Xie,
Wenlin Xu
Publication year - 2013
Publication title -
acta biochimica et biophysica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.771
H-Index - 57
eISSN - 1745-7270
pISSN - 1672-9145
DOI - 10.1093/abbs/gmt106
Subject(s) - pten , tensin , protein kinase b , cisplatin , pi3k/akt/mtor pathway , cancer research , microrna , cancer , kinase , transfection , chemistry , phosphatase , biology , microbiology and biotechnology , cell culture , signal transduction , phosphorylation , biochemistry , genetics , gene , chemotherapy
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.