摘要
目的研究表皮生长因子(EGF)对子宫内膜腺癌细胞系Ishikawa增殖的影响,并探讨雌激素受体α(ERα)和Ack1在其调控机制中的作用。方法无雌激素环境下,EGF作用于Ishikawa细胞,CCK-8法检测子宫内膜腺癌细胞增殖;Western blot检测细胞ERα及Ack1磷酸化;用酪氨酸激酶抑制剂达沙替尼处理细胞后,检测Ishikawa细胞增殖和ERα及Ack1磷酸化状态。结果 EGF可增强Ishikawa细胞增殖(P<0.05),并促进ERαTyr-537特异位点磷酸化和Ack1磷酸化;用达沙替尼后,细胞增殖能力下降(P<0.05),ERαTyr-537特异位点磷酸化和Ack1磷酸化水平下调。结论 EGF促进Ishikawa细胞增殖,其机制可能与诱导ERαTyr-537特异位点磷酸化和激活Ack1激酶通路有关。
Objective To investigate the effect of epidermal growth factor（ EGF） on the proliferation of endometrial adenocarcinoma cells,phosphorylation of estrogen receptor α（ ERα） and Ack1 in the absence of estrogen. Methods Ishikawa cell line was stimulated by EGF without estrogen settings,Cell Counting Kit-8（ CCK-8） was used to evaluate cell proliferation,Western blot was used to detect ER α phosphorylation and Ack1 phosphorylation. Giving tyrosine inhibitor dasatinib to assess the effect of EGF on cell proliferation,phosphorylation of ERα and Ack1 in Ishikawa cells. Results EGF enhanced the proliferation of endometrial adenocarcinoma cells（ P〈0. 05）. EGF induced ERα phosphorylation at Tyr-537 and phosphorylation of Ack1. Compared with untreated control,Dasatinib inhibited the proliferation of endometrial adenocarcinoma cells（ P〈0. 05）,phosphorylation of ERα Tyr-537 and Ack1. Conclusions EGF promotes Ishikawa cells proliferation in the possible way of activating ER α site-specific phosphorylation at Tyr-537 and phosphorylation Ack1,which could be blocked by dasatinib.
出处
《基础医学与临床》
CSCD
2017年第4期488-492,共5页
Basic and Clinical Medicine
基金
国家自然科学基金(81272842)
