Inhibitory effect of dihydroartemisinin on the growth of human prostate cancer PC-3M cells and its mechanism.
- Author:
Xin-Min WANG
1
;
Le ZHANG
;
Guo-Fu DING
;
Qin-Zhang WANG
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Artemisinins; pharmacology; Cell Line, Tumor; Cell Proliferation; drug effects; Flow Cytometry; Humans; Male; Prostatic Neoplasms; metabolism; pathology; Proto-Oncogene Proteins c-bcl-2; metabolism; RNA, Messenger; genetics; Vascular Endothelial Growth Factor A; metabolism
- From: National Journal of Andrology 2012;18(7):590-594
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effects of dihydroartemisinin on the apoptosis of and the vascular endothelial growth factor (VEGF) expression in prostate cancer cell line PC-3M in androgen-independent prostate cancer.
METHODSPC-3M cells were treated with different doses (0, 25, 50 and 100 micromol/L) of dihydroartemisinin for 48 hours, their growth activity analyzed by MTT colorimetric assay and flow cytometry, and changes in the activities of caspase-3 and -8 detected by colorimetric assay. The expression of VEGF mRNA was determined by semi-quantitative RT-PCR, and that of the VEGF protein by Western blotting.
RESULTSCompared with the 0 micromol/L control group, the 25, 50 and 100 micromol/L dihydroartemisinin groups showed significantly increased apoptosis of PC-3M cells ([2.92 +/- 0.45]% vs [8.85 +/- 0.74]%, [12.83 +/- 0.84]% and [18.65 +/- 1.24]%, P < 0.01), and dose-dependent increase in the activities of caspase-8 ([0.47 +/- 0.05 ] U/microg vs [1.22 +/- 0.15], [1.76 +/- 0.07] and [2.91 +/- 0.24] U/microg, P < 0.01) and caspase-3 ([0.44 +/- 0.07] U/microg vs [0.95 +/- 0.08], [1.48 +/- 0.14] and [2.92 +/- 0.45] U/microg, P < 0.01). The expressions of VEGF mRNA and protein were decreased in a concentration-dependent manner.
CONCLUSIONDihydroartemisinin can significantly suppress the growth of PC-3M cells, promote their apoptosis and reduce the expressions of VEGF mRNA and protein, which may serve to explain its inhibitory effect on tumor and angiogenesis.