期刊文献+

17-β雌二醇对人舌鳞癌细胞侵袭能力的影响及其机制探讨

17-β estradiol induces the invasion of human tongue squamous cell carcinoma via ERRα-FN pathway
下载PDF
导出
摘要 目的:探讨17-β雌二醇(E2)对人舌鳞癌细胞侵袭能力的影响及ERRα-FN通路在其中的作用。方法:以人舌鳞癌TCA8113细胞为研究模型,E2刺激模型细胞24 h;侵袭小室实验考察细胞的侵袭能力;ERRα特异性抑制剂XCT-790预处理模型细胞, siRNA转染干扰FN蛋白表达;蛋白质印记法检测FN蛋白表达水平。结果:E2(100 nmol/L)处理24 h能显著诱导TCA8113细胞侵袭率增加,上调FN蛋白表达(P<0.01);XCT-790预处理可降低E2诱导的细胞侵袭及FN蛋白表达(P<0.01);FN siRNA转染可沉默FN蛋白表达(P<0.01),并抑制E2对FN蛋白表达的诱导(P<0.01),抑制E2诱导的细胞侵袭(P<0.01)。结论:E2能诱导人舌鳞癌细胞侵袭能力增强,该作用与ERRα-FN通路信号通路有关。 Objective: To investigate the effect of 17-β estradiol (E2) on the invasion of human tongue squamous cell carcinoma cells and the role of ERRα-FN pathway. Methods: Model cells of TCA 8113 were stimulated by E2 for 24 h;the cell invasion was examined by invasion chamber assay. TCA 8113 cells treated by ERRa specific inhibitor XCT-790 were used as the pretreatment mod el cells;FN protein expression was interfered by FN siRNA;FN protein expression was detected by Western blot. Results: E2 (100 nmol/L) treatment for 24 h increased the invasion rate and up-regulated the FN protein expression in TCA8113 cells(P <0. 01). Pre treatment of TCA8113 cells by XCT-790 decreased E2-induced cell invasion rate and FN protein expression(P < 0. 01). FN siRNA transfection silenced FN protein expression in the cells(P <0.01), and inhibited the induction of FN expression by E2 (P < 0. 01). FN siRNA decreased the invasive rate induced by E2 (P < 0. 01). Conclusion: E2 can induce the invasion of human tongue squa mous carcinoma cells, which is related to the ERRa-FN pathway.
作者 陈英 钟雅静 曾钦 罗丽 CHEN Ying;ZHONG Yajing;ZENG Qin;LUO Li(The Third Branch of Chongqing People'Hospital,400014,China;Department of Stomatology,Second Affiliated Hospital of Army Military Medical University Chongqing)
出处 《实用口腔医学杂志》 CAS CSCD 北大核心 2019年第3期408-411,共4页 Journal of Practical Stomatology
关键词 17-β雌二醇(E2) 舌鳞状细胞癌 雌激素相关受体α(ERRα) 纤连蛋白(FN) 侵袭 17-β estradiol (E2) Tongue squamous cell carcinoma Estrogen related receptor a (ERRα) Fi bronectin (F/V) Invasion
  • 相关文献

参考文献3

二级参考文献17

共引文献26

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部