Abstract Title:

Bisphenol A promotes the proliferation of leiomyoma cells by GPR30-EGFR signaling pathway.

Abstract Source:

J Obstet Gynaecol Res. 2019 Apr 23. Epub 2019 Apr 23. PMID: 31016847

Abstract Author(s):

Zemin Li, Qing Lu, Bo Ding, Jingyun Xu, Yang Shen

Article Affiliation:

Zemin Li


AIM: To study the molecular mechanism of G protein-coupled receptor 30-epidermal growth factor receptor (GPR30-EGFR) signaling pathway on the proliferation of leiomyoma cells exposed with bisphenol A.

METHODS: Primary cultures and subcultures of human uterine leiomyoma (UL) cells. The expressions of messenger RNA and proteins of GPR30 and EGFR in 15 leiomyoma tissue specimens and all groups were detected by real-time quantitative polymerase chain reaction assay and Western blot assay. The protein of mitogen-activated protein kinases (MAPK)/extracellular signal-regulated kinases (ERK)/c-fos signaling pathway members was detected by Western blot assay.

RESULTS: Bisphenol A promoted the growth of UL cells and the expressions of GPR30, EGFR, c-fos and p-ERK1/2.

CONCLUSION: Bisphenol A was found to be a promoter specifically to proliferate the human UL cells by activating the transcription and translation of GPR30-EGFR and MAPK/ERK/c-fos signaling pathway members.

Study Type : In Vitro Study
Additional Links

Print Options

Key Research Topics

Sayer Ji
Founder of GreenMedInfo.com

Subscribe to our informative Newsletter & get Nature's Evidence-Based Pharmacy

Our newsletter serves 500,000 with essential news, research & healthy tips, daily.

Download Now

500+ pages of Natural Medicine Alternatives and Information.

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2020 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.