现代肿瘤医学
現代腫瘤醫學
현대종류의학
Journal of Modern Oncology
2015年
21期
3065-3068
,共4页
李青云%秦健%郝亚荣
李青雲%秦健%郝亞榮
리청운%진건%학아영
胃癌%雌二醇%细胞周期
胃癌%雌二醇%細胞週期
위암%자이순%세포주기
gastric cancer%estrogen%cell cycle
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。E 2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。
目的：初步探討雌二醇（ E2）對胃癌細胞SGC-7901增殖的影響。方法：SGC-7901細胞分為E2榦預組和對照組，E2榦預組加入不同濃度E2（0.1μmol/L、1.0μmol/L）榦預24小時，對照組加入等體積含無水乙醇的培養基。CCK8檢測E2對胃癌細胞增殖能力的影響，流式細胞術檢測細胞週期的分佈，PCR檢測E2對胃癌細胞雌激素受體ERα和ERβ mRNA錶達水平的影響，Oncomine公共數據庫查詢ERα的錶達情況。結果：E2對胃癌細胞的增殖抑製率具有濃度依賴性。E 2處理組 SGC -7901細胞G0/G1期細胞比例[（68.866±3.336）%]較對照[（59.333±0.294）%]顯著增加，G2期和S期細胞總比例下降，1.0μmol/L E2作用可使胃癌細胞SGC-7901髮生G1期阻滯（P﹤0.01）。兩種雌激素受體（ERα和ERβ）均錶達于胃癌細胞SGC-7901，且其相關基因ERα和ERβ mRNA錶達水平不隨E2濃度的增加而改變。利用Oncomine公共數據庫查詢髮現ERα在胃癌中的錶達高于癌徬。結論：E2直接作用可抑製胃癌細胞SGC-7901的增殖，引起G1期阻滯。
목적：초보탐토자이순（ E2）대위암세포SGC-7901증식적영향。방법：SGC-7901세포분위E2간예조화대조조，E2간예조가입불동농도E2（0.1μmol/L、1.0μmol/L）간예24소시，대조조가입등체적함무수을순적배양기。CCK8검측E2대위암세포증식능력적영향，류식세포술검측세포주기적분포，PCR검측E2대위암세포자격소수체ERα화ERβ mRNA표체수평적영향，Oncomine공공수거고사순ERα적표체정황。결과：E2대위암세포적증식억제솔구유농도의뢰성。E 2처리조 SGC -7901세포G0/G1기세포비례[（68.866±3.336）%]교대조[（59.333±0.294）%]현저증가，G2기화S기세포총비례하강，1.0μmol/L E2작용가사위암세포SGC-7901발생G1기조체（P﹤0.01）。량충자격소수체（ERα화ERβ）균표체우위암세포SGC-7901，차기상관기인ERα화ERβ mRNA표체수평불수E2농도적증가이개변。이용Oncomine공공수거고사순발현ERα재위암중적표체고우암방。결론：E2직접작용가억제위암세포SGC-7901적증식，인기G1기조체。
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 depen-denr 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 ex-pressed 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 ERαin 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.
