AKT2 reverses chemoresistance of ovarian cancer to cisplatin by regulating p27
10.3781/j.issn.1000-7431.2008.06.001
- Author:
Xiang TAO
1
Author Information
1. Molecular Cancer Center
- Publication Type:Journal Article
- Keywords:
Cells;
Cultured;
Oncogene protein v-akt;
Ovarian neoplasm;
P27;
RNA;
Small interfering
- From:
Tumor
2008;28(6):459-462
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To explore the role of v-akt murine thymoma viral oncogene homolog 2 (AKT2) and p27 in the chemoresistance of multicellular spheroids (MCS) of ovarian cancer to cisplatin. Methods: MCS of A2780 were formed by three-dimensional cell culture. Western blotting was applied to detect the expressions of AKT2 and p27. Then the interfering plasmid of AKT2 was constructed and transfected into the MCS of A2780 cells. The cell apoptosis after treatment with different concentrations of cisplatin was detected by flow cytometry (FCM) and the sensitivity of cells to cisplatin was evaluated by MTT assay. Results: Western blotting indicated that the expressions of AKT2 and p27 were higher in MCS than that in monolayer cells. The expressions of AKT2 and p27 in AKT2 shRNA-transfected MCS were significantly lower than that in MCS without transfection or transfected with empty vector. FACS analysis indicated that after treatment with various concentrations of cisplatin the apoptotic ratio of MCS was significantly lower than that in monolayer cells. AK72 shRNA transfection significantly increased the apoptotic ratio of MCS compared with those without transfection or transfected with empty vector. MTT assay showed that the sensitivity of MCS to cisplatin was increased after transfection with AK'12 shRNA. Conclusion: Interference with AKT2 shRNA down-regulated p27 and consequently reversed the drug resistance of ovarian cancer to cisplatin.
