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作 者:张根豪[1] 刘俊文[1] 苏利沙[2] 刘红春[1]
机构地区:[1]郑州大学第一附属医院检验科,郑州450052 [2]郑州大学第一附属医院产前诊断中心,郑州450052
出 处:《郑州大学学报(医学版)》2015年第2期240-243,共4页Journal of Zhengzhou University(Medical Sciences)
基 金:河南省教育厅重点科技攻关项目2013020036
摘 要:目的:研究阿司匹林对人卵巢癌组织和SKOV3细胞SOX7表达和Wnt/β-catenin信号通路的影响。方法:采用实时荧光定量PCR技术检测20例卵巢癌组织和20例正常卵巢组织中SOX7、β-catenin和Cyclin D1 mRNA的表达;0、0.5、1.0、2.0和3.0 mmol/L阿司匹林体外作用SKOV3细胞48 h后,采用实时荧光定量PCR技术检测细胞SOX7、β-catenin和Cyclin D1 mRNA的表达;MTT法检测0、0.5、1.0、2.0和3.0 mmol/L阿司匹林对SKOV3细胞增殖的影响。结果:与正常卵巢组织相比,卵巢癌组织中SOX7 mRNA表达降低(t=3.614,P=0.001),β-catenin和Cyclin D1 mRNA表达升高(t=13.651和5.967,P<0.001)。0、0.5、1.0、2.0和3.0 mmol/L阿司匹林作用48 h后,SKOV3细胞中SOX7 mRNA的表达水平逐渐升高(F=12.151,P<0.001),而β-catenin和Cyclin D1 mRNA的表达水平逐渐降低(F=6.214和4.903,P<0.05)。阿司匹林浓度依赖性地抑制SKOV3细胞的增殖(F=20.481,P<0.001)。结论:阿司匹林可能通过上调人卵巢癌中SOX7的表达对Wnt/β-catenin信号通路产生影响。Aim:To investigate the effect of aspirin on expression of SOX 7 and Wnt/β-catenin signaling pathway in hu-man ovarian cancer SKOV3 cells.Methods:The expression levels of SOX7,β-catenin and Cyclin D1 in ovarian tumor tissue and normal ovarian tissue were detected by quantitative real-time PCR( qRT-PCR) .The SKOV3 cells were stimulated by dif-ferent concentrations of aspirin in vitro and incubated for 48 h, then the expression of SOX 7,β-catenin and Cyclin D1 mRNA were detected by qRT-PCR.The effect of aspirin on SKOV3 cell proliferation was measured by MTT assay .Results:The ex-pression of SOX7 mRNA was decreased in ovarian cancer tissue (t=3.614,P=0.001),but the expressions of β-catenin and Cyclin D1 proteins were increased(t=13.651, 5.967, P〈0.001).The expression level of SOX7 mRNA was increased with the treatment of increasing concentration of aspirin (F=12.151,P〈0.001),but those of β-catenin mRNA and Cyclin D1 mRNA were decreased(F=6.214,4.903,P〈0.05) in SKOV3 cell.Aspirin inhibited the cell proliferation of SKOV3 cells in a concerntration-dependent manner(F=20.481,P〈0.001).Conclusion:Aspirin may have effect on Wnt/β-catenin sig-naling pathway by upregulating the expression of SOX 7 mRNA in human ovarian cancer SKOV3 cells.
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