双酚AF诱导乳腺癌细胞增殖的分子机制

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Abstract The effects of different concentrations of bisphenol AF (BPAF) on cell viability, cell cycle and apoptosis in MCF-7 In the study, breast cancer cells was evaluated. To evaluate cell proliferation mechanism, the novel estrogen membrane receptor G protein-coupled receptor 1 (GPER1)-mediated phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) and extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathways were used as targets. The effects of BPAF on the mRNA levels of related targets associated with PI3K/Akt and ERK1/2 signaling pathways were investigated and their roles in low concentration BPAF-induced breast cancer cell proliferation were analyzed. The results showed that low concentrations of BPAF (0.001~1μmol/L) significantly induced the cell proliferation, increased the proportion of S-phase cells and up-regulated mRNA levels of target genes in MCF-7cells. At high concentrations (>10 μmol/L), BPAF significantly inhibited cell viability and induced cell apoptosis. In addition, by using specific signal inhibitors, it was found that GPER1activated PI3K/Akt and ERK1/2 signaling pathways in mRNA level and activation of PI3K/Akt and ERK1/2 signaling pathways via GPER1 may be a key mechanism of BPAF-induced MCF-7 cell proliferation. ERα also plays an important role in this process.

Key words： bisphenol AF MCF-7 cells cell proliferation estrogen signaling pathways molecular mechanism

Received: 20 April 2021

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X503.1

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	LU Fen
	TANG Qian-qian
	LOU Shu-fang
	LEI Bing-li

Cite this article:

LU Fen,TANG Qian-qian,LOU Shu-fang等. Molecular mechanism of bisphenol AF-induced proliferation of breast cancer cells[J]. CHINA ENVIRONMENTAL SCIENCECE, 2021, 41(12): 5896-5903.

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http://www.zghjkx.com.cn/EN/ OR http://www.zghjkx.com.cn/EN/Y2021/V41/I12/5896

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