[Study on the inhibiting effects of equol on MCF-7 cells proliferation and its molecular mechanisms].

Abstract

OBJECTIVE:

To investigate the proliferation inhibition effects of equol on human breast cancer cell line MCF-7 and explore its molecular mechanisms.

METHODS:

MCF-7 cells were treated with different concentration of equol, including 0.1, 0.5, 1, 5 and 10 micromol/L. After the treatment, the proliferation rate of cells was examined by MTT method and the cell apoptosis percentage and cell cycle phase were determined by flow cytometry. The bag-1, bcl-2, VEGF, ERK1/2, p-ERK1/2, p38 and p-p38 protein were determined using Western blotting.

RESULTS:

A dose and time effect of proliferation inhibition of equol was proved in MCF-7. The MCF-7 cell apoptosis percentage increased significantly in the groups of equol, and the cell cycle arrest in G0/G1 phase. The expression of bag-1, bcl-2, VEGF, p-ERK1/2 and p-p38 protein were decreased gradually with the increase concentration of equol.

CONCLUSION:

The equol could inhibit the proliferation of the breast cancer cell lines MCF-7 and its inhibitory effect may be due to inducing apoptosis, arresting the cell cycle in G0/G1 phase, down-regulating the expression of bag-1, bcl-2, VEGF, p-ERK1/2 and p-p38 protein.

• Authors: Meng Wang, Guofeng Ren
• Journal: Wei sheng yan jiu = Journal of hygiene research (Wei Sheng Yan Jiu) Vol. 43 Issue 1 Pg. 11-5 (Jan 2014) ISSN: 1000-8020 [Print] China
• PMID: 24564104 (Publication Type: English Abstract, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• BCL2-associated athanogene 1 protein
• DNA-Binding Proteins
• Proto-Oncogene Proteins c-bcl-2
• Transcription Factors
• VEGFA protein, human
• Vascular Endothelial Growth Factor A
• Equol

Topics

• Apoptosis (drug effects)
• Cell Proliferation (drug effects)
• DNA-Binding Proteins (metabolism)
• Down-Regulation (drug effects)
• Equol (pharmacology)
• Female
• Humans
• MAP Kinase Signaling System
• MCF-7 Cells
• Proto-Oncogene Proteins c-bcl-2 (metabolism)
• Transcription Factors (metabolism)
• Vascular Endothelial Growth Factor A (metabolism)