雌激素对ERα-/ERβ-乳腺癌细胞增殖和侵袭的调节作用及分子机制  

Modulation Effect of Estrogen on Proliferation and Invasion of ERα-/ERβ-Breast Cancer Cells and Its Molecular Mechanisms

作　　者：陈坚平[1] 康凯夫[1] 周园园[1] 吴国标[1] 

机构地区：[1]顺德第一人民医院病理科,广东顺德528300

出　　处：《标记免疫分析与临床》2016年第4期459-462,共4页Labeled Immunoassays and Clinical Medicine

摘　　要：目的研究雌激素对ERα-/ERβ-乳腺癌细胞增殖和侵袭的调节作用及分子机制。方法选择乳腺癌细胞株SKBR-3(GPR30+,ERα-/ERβ-)进行研究,用不同水平的雌二醇进行处理,同时将GPR30的siRNA和阴性对照的siRNA转染进入细胞。处理24h后,检测细胞的增殖情况和侵袭情况。结果雌二醇处理能够以剂量依赖的方式增加细胞活力以及侵袭细胞的数目;转染GRP30-siRNA能够显著降低GPR30的mRNA含量,抑制效率为75.42%;雌二醇处理组的细胞活力以及侵袭数目均高于对照组,雌二醇联合GRP30-siRNA组的细胞活力以及侵袭数目均低于雌二醇处理组(P<0.05)。结论雌激素能够促进ERα-/ERβ-乳腺癌细胞的增殖和侵袭,受体GPR30可能是雌激素发挥作用的分子机制。Objective To study the modulation effect of estrogen on proliferation and invasion of ERα-/ ERβ-breast cancer cells and its molecular mechanisms. Methods Breast cancer cell line SK-BR-3（ GPR30 ＋,ERα-/ ERβ-） were collected for study. The cell line were treated with different concentrations of estradiol,while GPR30 siRNA and negative control siRNA were transfected into cells. After treatment for 24 h,cell proliferation and invasion were detected. Results Estradiol treatment can increase cell viability and invasive cells numbers by dose-dependent manner. Transfection of GRP30-siRNA can significantly reduce the content of GPR30 mRNA,inhibition efficiency was 75. 42%. Cell viability and invasive cells numbers of estradiol-treated group were higher than that in control group; cell viability and invasive cells numbers of estradiol combined with GRP30-siRNA group were lower than estradiol treated group（ P〈0. 05）. Conclusion Estrogen can promote ERα-/ERβ-breast cancer cell proliferation and invasion,estrogen receptor GPR30 may play a role in the molecular mechanism.

关 键 词：乳腺癌 雌激素 雌激素受体 GPR30 

分 类 号：R737.9[医药卫生—肿瘤]