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作 者:王娟[1] 刘青青 冯余宽 WANG Juan;LIU Qing-qing;FENG Yu-kuan(Department of Gynecology,Sichuan Fourth People s Hospital,Chengdu 610016,China;Department of Gynecology and Obstetrics,West China Second Hospital,Sichuan University,Chengdu 610041,China)
机构地区:[1]四川省第四人民医院妇科,四川成都610016 [2]四川大学华西第二医院妇产科,四川成都610041
出 处:《实用医院临床杂志》2019年第5期1-5,共5页Practical Journal of Clinical Medicine
摘 要:目的利用细胞模型检测雌激素及雌激素受体对卵巢癌的影响,初步探讨其机制。方法以不同浓度的雌激素处理卵巢癌细胞系A2780和OVCAR3,利用细胞增殖实验和细胞克隆成形实验检测雌激素对细胞增殖和成瘤能力的影响,划痕实验检测雌激素对细胞迁移的影响。使用过表达载体和基因沉默进行功能获得和功能缺失实验。荧光实时定量PCR检测相关基因的表达。结果1 nM的雌激素处理不影响A2780和OVCAR3细胞的增殖,但100 nM的雌激素处理可以抑制A2780和OVCAR3细胞的增殖和迁移。雌激素处理可以下调MALAT-1的表达,分别在ERα和ERβ缺失的细胞系中检测MALAT-1表达水平,发现雌激素是通过ERα下调MALAT-1的转录。结论高浓度的雌激素以ERα受体-依赖的方式下调长链非编码RNA MALAT-1的表达,抑制卵巢癌细胞的增殖和迁移。Objective To investigate the effects of estrogen and estrogen receptor on ovarian cancer with a cell model and to preliminarily explore its mechanism.Methods The ovarian cancer cell lines A2780 and OVCAR3 were treated with different concentrations of estrogen.The effects of estrogen on cell proliferation and tumorigenesis were detected by using cell proliferation test and cell clone formation test,and the effects of estrogen on cell migration were detected by using scratch test.Overexpression vector and gene silencing were used for functional acquisition and functional deletion experiments.The expression of related genes was detected by real-time quantitative fluorescence PCR.RessIts Estrogen treatment of 1 nM did not affect the proliferation of the cells,but estrogen treatment of 100 nM inhibited the proliferation and migration of the cells.Estrogen treatment could down-regulate the expression of MALAT-1.The expression of MALAT-1 was detected in ER-αand ER-αdeleted cell lines,respectively.It was found that estrogen down-regulated the transcription of MALAT-1 through ER-α.a.Conclusion High concentration of estrogen can down-regulate the expression of long-chain non-coding RNA of MALAT-1 in an ER-αreceptor-dependent manner and inhibit the proliferation and migration of ovarian cancer cells.
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