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作 者:魏翻艳[1] 李郁[2] 陈必良[1] 董曦文 吴娟[1] 杨红[1]
机构地区:[1]第四军医大学西京医院妇产科,陕西西安710032 [2]第四军医大学细胞工程研究中心,陕西西安710032
出 处:《现代生物医学进展》2014年第14期2610-2614,共5页Progress in Modern Biomedicine
基 金:国家自然科学基金项目(81072144)
摘 要:目的:研究上皮性卵巢癌细胞中FOXM1的表达,探讨FOXM1与MMP9之间的相关性以及与卵巢癌细胞侵袭、转移的关系。方法:采用Real-time RT-PCR、Western blotting技术检测pcDNA3.1-FOXM1和FOXM1-siRNA分别转染卵巢癌细胞株HO-8910(低转移)和HO-8910PM(高转移)前后FOXM1的表达水平,用Transwell方法检测转染该序列后HO-8910和HO-8910PM细胞侵袭能力的改变,并用荧光素酶双报告基因分析技术检测FOXM1对MMP9的调控作用。结果:与对照组和空载组相比,转染了pcDNA3.1-FOXM1的HO-8910细胞FOXM1 mRNA、蛋白表达显著升高,而转染了FOXM1-siRNA的高转移细胞株HO-8910PM FOXM1 mRNA、蛋白表达显著降低(P<0.05);相对于空载体组和空白组,pcDNA3.1-FOXM1转染组细胞的侵袭能力明显增强,而FOXM1-siRNA转染细胞的侵袭能力明显降低(P<0.05);FOXM1参与对MMP9的转录调控作用(P<0.05)。结论:FOXM1可能是一个潜在的治疗靶点,通过下调FOXM1的表达,从而抑制卵巢癌的浸袭和转移。Objective: The expression of FOXMI in epithelial ovarian cancer cell was investiageted to learn the relationship between FOXMI and MMP-9 as well as its role in the invasiveness of ovarian cancer cell. Methods: Rea1-time RT-PCR and Western blotting were performed to detect the expression levels of FOXM1 before and after overexpression vectors pcDNA3.1-FOXM1 and FOXM1 siRNA were transfected into HO-8910 and HO-8910PM cells respectively. The change of invasion capacity was evaluated by Transwell chamber test. The involvement of FOXM1 in regulating MMP9 expression was explored by Dual-luciferase reporter assay system. Results: After overexpression vectors pcDNA3.1-FOXM1 was transfected into HO-8910, FOXM1 expression at both mRNA and protein levels were significantly increased and the invasion capacity of ovarian cancer cells was obviously enhanced compared to the control group(P〈0.05). After FOXM1 siRNA was transfected into HO-8910PM, FOXM1 expression at both mRNA and protein levels were significantly decreased and the invasion capacity of ovarian cancer cells was obviously reduced compared to the control group(P〈0.05). FOXM1 was involved in the transcription regulation of MMP9(P〈0.05). Conclusion: FOXM1 may serve as a promising therapeutic target for ovarian cancer. The invasion capacity of ovarian cancer cells can be inhibited through down-regulating FOXM1.
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