Apoptosis induced by cantharidin in human pulmonary carcinoma cells A549 and its molecular mechanisms.
- Author:
Wei-dong ZHANG
1
;
Hui-ru ZHAO
;
Ying YAN
;
Xiao-hua WANG
;
Zhi-hong ZONG
;
Ying LIU
Author Information
- Publication Type:Journal Article
- MeSH: Adenocarcinoma; pathology; Antineoplastic Agents; pharmacology; Apoptosis; drug effects; Cantharidin; pharmacology; Cell Line, Tumor; Humans; Inhibitor of Apoptosis Proteins; Lung Neoplasms; pathology; Microtubule-Associated Proteins; biosynthesis; genetics; Neoplasm Proteins; biosynthesis; genetics; Proto-Oncogene Proteins c-bcl-2; biosynthesis; genetics; bcl-2-Associated X Protein; biosynthesis; genetics
- From: Chinese Journal of Oncology 2005;27(6):330-334
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the apoptosis-inducing effect of cantharidin in human lung cancer cells A549 and its molecular mechanisms.
METHODSMTT assay was used to determine A549 cells proliferation. Light and electron microscopy, FACScan, Annexin V-FITC staining and DNA gel electrophoresis were used to detect apoptosis. The expression of bcl-2, Bax and survivin were examined by Western blot.
RESULTSCantharidin inhibited the proliferation of A549 cells. The cells treated with cantharidin showed a typical apoptotic morphology and hypodiploid peak before G(1) phase. Flow cytometry analysis with annexin quantitatively further confirmed the increase of cell apoptosis. DNA of treated A549 cells depicted a ladder pattern characteristic of apoptosis, indicating the presence of DNA fragmentation. Western blot assay showed that cantharidin increased the level of Bax expression and inhibited the level of bcl-2 and survivin expression.
CONCLUSIONCantharidin can induce A549 cells apoptosis mainly via regulation of Bax, bcl-2 and survivin expression.
