雌二醇对胃癌细胞周期的影响

目的:初步探讨雌二醇（E2）对胃癌细胞SGC-7901增殖的影响。方法:SGC-7901细胞分为E2干预组和对照组，E2干预组加入不同浓度E2（0.1μmol/L、1.0μmol/L）干预24小时，对照组加入等体积含无水乙醇的培养基。CCK8检测E2对胃癌细胞增殖能力的影响，流式细胞术检测细胞周期的分布，PCR检测E2对胃癌细胞雌激素受体ERα和ERβ mRNA表达水平的影响，Oncomine公共数据库查询ERα的表达情况。结果:E2对胃癌细胞的增殖抑制率具有浓度依赖性。E2处理组SGC-7901细胞G0/G1期细胞比例［(68.866±3.336)%］较对照［(59.333±0.294)%］显著增加，G2期和S期细胞总比例下降，1.0μmol/L E2作用可使胃癌细胞SGC-7901发生G1期阻滞（P<0.01）。两种雌激素受体（ERα和ERβ）均表达于胃癌细胞SGC-7901，且其相关基因ERα和ERβ mRNA表达水平不随E2浓度的增加而改变。利用Oncomine公共数据库查询发现ERα在胃癌中的表达高于癌旁。结论:E2直接作用可抑制胃癌细胞SGC-7901的增殖，引起G1期阻滞。

The effect of estradiol on cell cycle distribution of gastric cancer cell

Objective:To investigate the effect of estradiol (E2） on gastric cancer cell SGC-7901.Methods:SGC-7901 cell was treated with or without E2 for 24 hours.Cell Counting Kit-8 (CCK8） was applied for evaluation of impact of E2 on gastric cancer cell proliferation.The cell cycle distribution was analyzed by flow cytometry.mRNA expression level of ERα and ERβ of E2-treated gastric cancer cell was analyzed by PCR.Oncomine database query the expression of ERα.Results:E2 treatment significantly inhibited gastric cancer cell proliferation in a dose dependenr manner.Cell number of G1 phase was obviously increased by E2 treatment (68.866±3.336)% as compared with blank control group (59.333±0.294)%，while G2 and S phase cell proportion was reduced.1.0μmol/L E2-treatment induced a cell cycle arrest at G1 phase (P<0.01).The two receptors of estrogen were consistently expressed in gastric cancer cells and no changes on mRNA expression levels of ERα or ERβ were deceted during E2 treatment.Oncomine database showed the expression of ERα in gastric cancer was higher than non-cancerous tissue.Conclusion:Estrogen can inhibit cell proliferation and induce cell cycle arresting in G1 phase in gastric cancer cell directly.