| 茅昌飞 1 唐金海 1 △ 孙大伟 2 吴建中.BPA 激活 GPER-EGFR-ERK1 /2 信号通路诱导乳腺癌细胞增殖[J].现代生物医学进展英文版,2015,15(6):1024-1027. |
| BPA 激活 GPER-EGFR-ERK1 /2 信号通路诱导乳腺癌细胞增殖 |
| Involvement of GPER-EGFR-ERK1 /2 in Bisphenol A Induced Breast CancerCell Proliferation |
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| DOI： |
| 中文关键词: 双酚 A GPER 乳腺癌 细胞增殖 |
| 英文关键词: Bisphenol A GPER Breast cancer Proliferati |
| 基金项目: |
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| 中文摘要: |
| 目的： 研究雌激素 G 蛋白 偶联受体（ G protein-coupled estrogen receptor， GPER）- 表皮生长因子受体( epidermal growthfactor
receptor， EGFR)- 细胞外调节蛋白 激酶 1/2 (extracellular regulated protein kinases, ERK)信号通路在双酚 A 促乳腺癌细胞 SKBR-3
增殖中的作用 。方法： 采用 CCK8 试剂盒检测 SKBR-3 细胞的增殖情况， 利用 Western Blot 观察 ERK1 /2 磷酸化变化。结果： 与 对照
组相比， 10-11～ 10-7 M 浓度的双酚 A 具有促乳腺癌细胞增殖作用 ， 10-9M 浓度的双酚 A 可诱导细胞增殖最大效应（细胞活力高于对
照组约 38.84 %， P<0.001）；预孵 GPER、 EGFR、 ERK1/2 特异性抑制 剂 G15、 AG-1478、PD98059 后， 双酚 A 诱导的乳腺癌细胞增殖
明 显减少， 细胞活力 与单纯双酚 A（ 10-9 M）处理相比降低约 1 4.27 %、12.23 %和 17.98 %（ P<0.05）； 双酚 A（ 10-9 M）处理细胞 0.5、 1、
3 小时后， 发现磷酸化的细胞外信号调节激酶（ p-ERK）的 表达明 显高于对照组， 双酚 A 可快速激活 ERK1 /2； 而阻断 GPR30 和
EGFR 后， ERK1 /2 的磷酸化表达减少。 结论： 双酚 A 诱导的乳腺癌细胞增殖可能与 GPR30-EGFR-ERK1 /2 信号通路有关， 但不是
唯一通路。 深入研究双酚 A 对促进乳腺癌细胞增殖机制， 可能为 乳腺癌的防治提供新的方向。 |
| 英文摘要: |
| Objective:To explore the effect of Bisphenol A on the proliferation of human breast cancer cells (SKBR-3) via
GPER-EGFR-ERK1/2 signaling pathway.Methods:CCK8 assay was used to detect the proliferation of SKBR-3 cells, and Western
Blotting was applied to observe phosphorylation of ERK1/2.Results:Cell proliferation increased significantly with treatment of 10-11-10-7
M BPA after 24 h, and 10-9 M BPA can induce cell proliferation maximum effect (cell viability higher approximately 38.84 % compared
with the control, P<0.001 ); with pre-incubation of G15, AG-1478 and PD98059 (specific antagonist of GPER, EGFR and ERK1 /2), cell
proliferation decreased remarkably. Cell viability had a decrease of approximately 14.27 %, 1 2.23 % and 17.98 % compared with BPA
(10-9 M) treatment (P<0.05); 0.5, 1, 3 h after BPA (10-9 M) treatment, phosphorylated extracellular signal-regulated kinase (p-ERK)
expression increased significantly， indicating that ERK 1 /2 was activated rapidly; after blocking GPR30 and EGFR, ERK 1 /2
phosphorylation decreased.Conclusion:GPR30-EGFR-ERK 1/2 signaling pathway was involved in BPA-induced breast cancer cell
proliferation. In-depth research of BPA to breast cancer cell proliferation may provide a new direction for the prevention and treatment of
breast cancer. |
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