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卵巢癌细胞中ERK1/2的表达及其与细胞凋亡的关系 被引量:2

The expression of ERK1/2 in ovarian carcinoma cell and its correlation with apoptosis
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摘要 目的研究细胞外信号调节激酶ERK1/2在卵巢癌细胞SKOV3中的表达及其与细胞相关凋亡蛋白的关系。方法用MTT检测17β-E2对细胞的增殖情况,用MEK1/2通路抑制剂U0126在不同浓度、不同时间处理细胞后,RT-PCR检测细胞ERK1 mRNA、ERK2 mRNA、caspase-3 mRNA的表达。结果浓度为10-6mol/L17β-E2作用1h可显著促进细胞增殖[(5.7±0.23)%],与对照组[(3.5±0.45)%]相比,P=0.000。ERK1/2在卵巢癌中高表达,随着U0126处理细胞浓度的增加及时间的延长,ERK1的表达逐渐降低,与对照组相比,P值分别为0.176、0.009、0.002、0.000;ERK2的表达逐渐降低,与对照组相比,P值分别为0.010、0.000、0.000、0.000;caspase-3的表达逐渐增加,与对照组相比,P值分别为1.000、0.290、0.090、0.003。结论 ERK1/2与卵巢癌的发生发展有关,抑制ERK1/2的表达可抑制细胞增殖,增加细胞凋亡。 Objective To investigate the expression of extracellular signal-regulated kinasel/2 (ERK1/2) in ovarian carcinoma cell and its correlation with apoptosis. Methods The proliferation was assayed by MTr when the cells were exposed to 17β-E2. After the cell was treated with U0126 which is MEK suppressor,the expression of caspase-3, ERK1, ERK2 mRNA in ovarian carcinoma cell were detected by RT-PCR in different concentration and different time. Results The cell proliferative rate was significantly higher [ (5.7 ± 0.23 ) % ] after stimulation with 17β-E2 at 1 × 10^-6 mol/L for 60 rain than control[ (3.5 ±0. 45)% ] (P =0. 000). ERK1/2 was highly expressed, after the cell were treated with U0126 ,along with increasing of time and concentration,the expression of ERK1 was increasingly reduction, compared to control group, P = 0. 176,0. 009,0. 002,0. 000 ; the expression of ERK2 was increasingly reduction too, compared to control group, P = 0. 010,0. 000,0. 000,0. 1300; while the expressior± of caspase-3 were increasingly highly than control, P = 1. 000, 0. 290, 0. 090, 0. 003. Conclusion ERK1/2 is participate in the occurrence and development of ovarian cancer. When ERK1/2 expression is inhibited, cell proliferation is inhibited,while cell apoptosis is increased.
出处 《中华临床医师杂志(电子版)》 CAS 2013年第9期124-126,共3页 Chinese Journal of Clinicians(Electronic Edition)
关键词 卵巢肿瘤 细胞外信号调节MAP激酶类 细胞凋亡 Ovarian neoplasms Extracellular sigual-regulated MAP kinases Apoptosis
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