目的：研究雌激素受体（estrogen receptor，ER）亚型对人乳腺癌细胞MCF7的生长及Th1/Th2类细胞因子分泌的影响。方法：采用RNA干扰技术沉默MCF7细胞中ERα或ERβ的表达，获得ERα/ERβ不同表达状态的MCF7细胞。应用MTT法、流式细胞术、RTPCR法分别检测MCF7细胞的增殖、细胞周期和凋亡抑制基因的表达，ELISA法检测细胞上清中IFNγ和IL4的分泌水平。结果：经RNA干扰后MCF7细胞的ERα或ERβ蛋白表达水平分别下降了（77.7±3.3）%和（68.3±2.1）%。与对照组相比，ERα基因沉默后，MCF7细胞生长减慢（P<0.05），受阻于G0～G1期，凋亡抑制基因XIAP的表达水平降低为对照组的（43.0±2.0）%，IFNγ分泌水平增加至对照组的（1.89±0.34）倍；ERβ基因沉默促进MCF7细胞的生长（P<0.05），S期细胞比例增加，凋亡抑制基因Bcl2、Bclxl、XIAP 的表达水平分别升高至对照组的（1.28±0.21）、（161±0.32）和（1.65±0.29）倍，IFNγ分泌水平降低为对照组的（28.0±4.0）%。结论：ER亚型的表达状态可影响MCF7细胞的生长，并通过调节IFNγ的自分泌水平诱导微环境发生Th偏移。

Objective:To study estrogen receptor (ER) subtype on the growth of breast cancer cell line MCF7 and the secretion of Th1 and Th2 cytokines in MCF7 tumor microenvironment. Methods: ERα or ERβ expression in MCF7 cells was silenced by RNA interference and MCF7 cells with different ERα/ERβ expression status were obtained. MTT test, flow cytometry and RTPCR assay were used to detect proliferation, cell cycle and expression of apoptosis suppressor genes. Secretion of IFNγ and IL4 in cell supernatant were analyzed by ELISA assay. Results: After RNA interference, protein levels of ERα or ERβ in MCF7 cells decreased by (77.7± 3.3 )% or (68.3±21)%, respectively. Compared to control group, after knocking down ERα gene expression, MCF7 cells grew slower (P＜0.05) and were arrested at phase G0～G1, expression of apoptosis suppressor gene XIAP decreased by (43.0±2.0)%. and the level of IFNγ increased by (1.89±0.34) times. However, after knocking down the ERβ gene expression, MCF7 grew faster (P<005), and the proportion of cells entering S phase increased, the expression of apoptosis suppressor genes Bcl2, Bclxl and XIAP increased by (1.28±0.21) times, (1.61±0.32) times and (1.65±0.29) times, respectively, while the level of IFNγ decreased by (28.0±4.0)%, compared to the control group. Conclusion: The expression status of ER subtype can affect the growth of MCF7 cells and induce the Th bias in microenvironment by regulating the autocrine level of IFNγ.

国家自然科学基金资助项目（No.81041071）；天津市自然科学基金资助项目(No.08JCYBJC06900)；武警医学院科学技术研究面上项目资助（No.WY200802）