Inhibitory effect of sodium valproate on human lung carcinoma SPC-A1 cell proliferation and the mechanism.
- Author:
Zhihong HUANG
1
;
Qing CHEN
;
Liuhong MA
;
Zhiming CHEN
;
Wenpu CHEN
;
Li QIN
;
Jianwei JIANG
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Caspase 3; metabolism; Caspase 9; metabolism; Cell Line, Tumor; Cell Proliferation; drug effects; Humans; Myeloid Cell Leukemia Sequence 1 Protein; Proto-Oncogene Proteins c-bcl-2; metabolism; Valproic Acid; pharmacology; bcl-X Protein; metabolism
- From: Journal of Southern Medical University 2012;32(5):606-609
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of sodium valproate (VPA) on the proliferation and apoptosis of human lung carcinoma SPC-A1 cells and the underlying mechanism.
METHODSThe effect of VPA on the proliferation of SPC-A1 cells was evaluated by MTT assay and clone formation assay. Flow cytometry was used to analyze the apoptosis of the cells exposed to VPA. The changes in the expressions of Bcl-xl, Bcl-2, Mcl-1, caspase-9, and caspase-3 in the exposed cells were detected by Western blotting.
RESULTSIncubation with VPA for 48 h resulted in a significant inhibition of SPC-A1 cell proliferation, with a IC(50) of 1.8 mmol/L. VPA treatment also inhibited cell colony formation and induced obvious cell apoptosis. Exposure to 8 mmol/L VPA for 48 h caused a percentage of early apoptotic cells of 60.44%. VPA treatment at different concentrations for 48 h obviously lowered the protein levels of Bcl-xl, Bcl-2, and Mcl-1 and induced caspase-9 and caspase-3 activation in SPC-A1 cells.
CONCLUSIONVPA can inhibit the proliferation of SPC-A1 cells by triggering mitochondrion-dependent apoptosis.
