雌二醇通过雌激素β受体促进非小细胞肺癌A549细胞增殖

17β-estradiol promotes proliferation of NSCLC cells A549 via estrogen receptor β

目的观察雌二醇(E2)激动雌激素受体ERα和ERβ时,对非小细胞肺癌(NSCLC)细胞增殖能力的影响。方法将A549细胞和H1299细胞分别用E2、雌激素α受体激动剂(PPT)和雌激素β受体激动剂(DPN)处理24 h和48 h。利用MTT法筛选出三者在NSCLC细胞系A549和H1299中对细胞增殖产生作用的有效浓度和时间;利用平板克隆形成实验检测E2、PPT、DPN对A549和H1299的细胞增殖能力的影响;利用流式细胞术检测E2、DPN对A549的细胞凋亡和细胞周期的影响。结果 MTT实验和平板克隆实验结果显示E2及DPN能够促进A549细胞的增殖(P <0. 05),而二者均不能促进H1299细胞的增殖(P> 0. 05),二者的最佳作用浓度为10^(-8)mol/L。而PPT在高浓度时严重抑制两种细胞的增殖(P <0. 05),低浓度时则对两种细胞的增殖无明显的促进作用(P> 0. 05)。流式细胞术结果提示E2和DPN通过促进细胞G1-S周期进程,提高A549细胞增殖能力(P <0. 05),而对A549细胞凋亡没有影响(P> 0. 05)。结论 E2和DPN均可促进A549细胞的增殖,但是PPT不能促进A549细胞的增殖,提示雌二醇通过激活雌激素β受体促进A549细胞的增殖。

Objective To explore the effects of17β-estradiol(E2)on proliferation of non-small cell lung cancer(NSCLC)cells after activating estrogen receptor ERαand ERβ.Methods A549 cells and H1299 cells were treated with E2,ERαagonist(PPT)or ERβagonist(DPN)for 24 h and 48 h,respectively.MTT assay was used to screen out their effective concentration and time in which E2,PPT and DPN promoted proliferation of NSCLC A549 cells and H1299 cells.The effects of E2,PPT and DPN on proliferation of A549 cell and H1299 cell were observed using plate clone formation assay.The effects of E2 and DPN on apoptosis and cell cycle of A549 were observed by flow cytometry.Results E2 and DPN promoted proliferation of A549 cell by MTT assay and plate clone formation assay(P<0.05),and the best effective concentration was10-8 mol/L.But E2 and DPN did not promote proliferation of H1299 cells(P>0.05).Meanwhile,PPT suppressed proliferation of A549 cells and H1299 cells in higher concentrations(P<0.05),and did not promote the proliferation in lower concentrations(P>0.05).Flow cytometry showed that E2 and DPN promoted proliferation of A549 cells through promoting G1-S phase of cell cycle(P<0.05),but they did not work in apoptosis of A549 cells.Conclusion E2 and DPN could both promote proliferation of A549 cells,but PPT could not.The results suggest that E2 could promote proliferation of A549 cell via activating ERβ.