Crypotanshione reduces the expression of metadherin in DU145 prostate cancer cells.
- Author:
Yi YAO
;
Hui-zhang LI
;
Ben-jiang QIAN
;
Chang-ming LIU
;
Jia-bin ZHANG
;
Miao-chun LIN
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Cell Adhesion Molecules; metabolism; Cell Line, Tumor; Cell Proliferation; drug effects; Diterpenes, Abietane; pharmacology; Down-Regulation; Drugs, Chinese Herbal; pharmacology; Humans; In Situ Nick-End Labeling; Male; Neoplasm Proteins; metabolism; Phosphatidylinositol 3-Kinases; metabolism; Prostatic Neoplasms; metabolism; pathology; Proto-Oncogene Proteins c-akt; metabolism; Proto-Oncogene Proteins c-bcl-2; metabolism; RNA, Messenger; metabolism; Signal Transduction; drug effects; Time Factors
- From: National Journal of Andrology 2015;21(9):782-787
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of crypotanshinone (CPT) on the proliferation and apoptosis of DU145 prostate cancer cells as well as on the metadherin expression and the downstream PI3K/AKT signaling pathway in the DU145 cells.
METHODSWe treated DU145 prostate cancer cells with different concentrations of CPT for 24, 48, and 72 hours followed by evaluation of the proliferation and apoptosis of the cells by MTT assay and TUNEL, respectively. We determined the expressions of metadherin protein and mRNA in the DU145 cells by Western blot and RT-PCR respectively at different time points after CPT treatment. We also detected the expressions of the proteins metadherin, AKT, p-AKT, and Bcl-2 in the CPT-treated DU145 cells at 48 hours.
RESULTSCPT significantly inhibited the proliferation of the DU145 cells in a dose- and time-dependent manner (P < 0.05). After treatment with 10 µmol/L CPT for 24, 48, and 72 hours, the apoptosis rates of the DU145 cells were (29.42 ± 4.51), (55.07 ± 5.67) and (70.84 ± 4.66)%, respectively, significantly higher than (3.1 ± 2.48)% in the control group (P < 0.05). The expression of metadherin was remarkably downregulated at the transcription and translation levels (P < 0.05) and the expressions of the AKT signaling pathway and the Bcl-2 protein were markedly inhibited in the DU145 cells after treated with 10 µmol/L CPT for 48 hours (P < 0.05).
CONCLUSIONCPT can inhibit the proliferation and induce the apoptosis of DU145 prostate cancer cells, which may be associated with its suppression of the downstream PI3K/AKT signaling pathway by reducing the expression of metadherin in the DU145 cells.