NDLI: Effect of bisphenol A on the EGFR-STAT3 pathway in MCF-7 breast cancer cells.

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Effect of bisphenol A on the EGFR-STAT3 pathway in MCF-7 breast cancer cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Fang, Yanqiu Tan, Yan Zhang, Minglei Shi, Xu Zhang, Wei Wang, Xiaoqi
Description	Author Affiliation: Zhang W ( Research Center, The First Clinical Hospital of Jilin University, Jilin 130021, PR China.)
Abstract	The aim of this study was to explore the effect of bisphenol A (BPA) on the EGFR-STAT3 pathway in breast cancer. We applied 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide (MTT) cytotoxicity assay to the analysis of the responsiveness of MCF-7 cells to BPA. Gene expression was assayed at the transcriptional and translational levels by reverse transcription-PCR and Western blotting. We explored the effects of BPA on MCF-7 cell proliferation through inhibition of the related genes, STAT3, using RNA interference, and EGFR, using its inhibitor AG1478. The optimal concentration and time point of BPA-induced proliferation in MCF-7 cells are 1 µM and 24 h, respectively. BPA significantly increased the expression of STAT3 at a concentration of 1 µM following treatment for 48 h and the expression of STAT3 was down-regulated after blocking EGFR. When STAT3 was blocked in MCF-7 cells, BPA did not appear to induce cell proliferation. Treatment with BPA (1 µM) in the presence of AG1478 for 48 h resulted in the stimulation of cell growth in MCF-7 cells, similar to that of the BPA alone treatment. BPA increases STAT3 expression, which is a major factor in the pathway of BPA-induced proliferation, and STAT3 activation contributes to BPA-induced breast cancer cell proliferation. However, EGFR mediates negative signaling for BPA-induced breast cancer cell proliferation.
ISSN	17912997
e-ISSN	17913004
Journal	Molecular Medicine Reports
Issue Number	1
Volume Number	5
Language	English
Publisher	Spandidos Publications
Publisher Date	2012-01-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Phenols Pharmacology Receptor, Epidermal Growth Factor Metabolism Stat3 Transcription Factor Benzhydryl Compounds Breast Neoplasms Cell Line, Tumor Cell Proliferation Drug Effects Gene Expression Regulation, Neoplastic Quinazolines Rna Interference Rna, Small Interfering Antagonists & Inhibitors Genetics Signal Transduction Time Factors Tyrphostins Research Support, Non-u.s. Gov't Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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