miR-29b Reduces Cisplatin Resistance of Gastric Cancer Cell by Targeting PI3K/Akt Pathway.
- Author:
Dian-dian CHEN
1
;
Lin-chun FENG
1
;
Rui YE
2
;
Yu-qi HE
;
Ya-di WANG
Author Information
- Publication Type:Journal Article
- MeSH: Blotting, Western; Cell Line, Tumor; Cell Survival; Cisplatin; Down-Regulation; Drug Resistance, Neoplasm; Humans; MicroRNAs; Phosphatidylinositol 3-Kinases; Signal Transduction; Stomach Neoplasms; Up-Regulation
- From: Acta Academiae Medicinae Sinicae 2015;37(5):514-519
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the regulatory effect of miR-29b on gastric cells' resistance to cisplatin.
METHODSThe expression of miR-29b in gastric cancer cell line treated with cisplatin concentration gradient was detected using quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) and Western blotting. CCK8 was used to measure the cell viability after cisplatin treatment in condition of miR-29b knock-down and overexpression.
RESULTSThe expression of miR-29b was significantly upregualted by cisplatin treatment,while its target gene AKT2 was downregulated. The up-regulation of miR-29b enhanced the sensitivity of gastric cancer cells to cisplatin,while the knock-down of miR-29b enhanced the cisplatin resistance. Rescue experiments demonstrated that the miR-29b might regulate cisplatin resistance of gastric cancer cell by targeting PI3K/Akt pathway. The expressions of the other two members of miR-29 family, miR-29a/c, were promoted by cisplatin treatment,but they had no significant effect on gastric cancer cell's resistance to cisplatin.
CONCLUSIONmiR-29b can enhance the sensitivity of S gastric cancer cell by directly targeting PI3K/Akt pathway.
