Effects of zearalenone on proliferation and apoptosis in MCF-7 cells.
- Author:
Zeng-li YU
1
;
Li-shi ZHANG
;
De-sheng WU
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Blotting, Western; Breast Neoplasms; genetics; metabolism; pathology; Cell Cycle; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Estrogens, Non-Steroidal; pharmacology; Female; Flow Cytometry; Humans; Proto-Oncogene Proteins c-bcl-2; biosynthesis; genetics; Reverse Transcriptase Polymerase Chain Reaction; Zearalenone; pharmacology; bcl-2-Associated X Protein; biosynthesis; genetics
- From: Chinese Journal of Preventive Medicine 2005;39(5):328-331
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effects of zearalenone (ZEA) on proliferation and apoptosis in estrogen-dependent human breast cancer MCF-7 cells and the likely underlying molecular mechanisms.
METHODSCell viability was determined by MTT assay and cell cycle distribution by cytometry. Apoptosis was detected by Cell Death Detection ELISA and cytometry, respectively. The expressions of bax and bcl-2 were examined using multiple RT-PCR and Western-blot both at mRNA and protein level, respectively.
RESULTSThe current study confirmed the previous studies that ZEA could stimulate proliferation in MCF-7 cells with inducing a profound increase in S phase and a modest increase in G(2)/M phase that was accompanied by a decrease in G(0)/G(1) phase. ZEA could inhibit apoptosis in MCF-7 cells following estrogen ablation at a range of concentrations of 2 nmol/L -96 nmol/L. Western blot and RT-PCR analysis revealed that the anti-apoptotic bcl-2 was upregulated at both protein and mRNA level, together with the downregulation of pro-apoptotic bax.
CONCLUSIONZEA should have possessed comparative estrogenic activity and could promote the progression of MCF-7 cells through the cell cycle by a decreasing in the G(0)/G(1) phase and by a significant increasing in S-phase. The pro-proliferative activity of ZEA was due to inhibition of apoptosis through regulation of bax/bcl-2 expression.