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作 者:刘尚辉[1] 姜琳琳[2] 张海燕[2] 邓娓娓[2] 王华芹[1]
机构地区:[1]中国医科大学基础医学院,辽宁沈阳110001 [2]中国医科大学附属第一医院老年病科,辽宁沈阳110001
出 处:《中国现代医学杂志》2014年第29期8-12,共5页China Journal of Modern Medicine
基 金:国家自然基金资助项目青年基金(No:81301838)
摘 要:目的 研究蛋白酶体抑制剂对人甲状腺癌细胞中过氧化氧化还原蛋白(PRDXs)表达的影响及其机制。方法 选取人甲状腺癌细胞,设立对照组和蛋白酶体抑制剂处理组;用实时定量聚合酶链反应(RT-PCR)、免疫印迹(Wester blot)检测PRDXs在各组甲状腺癌细胞中的表达。结果 与对照组相比,MG132处理组中PRDX1 mRNA、蛋白和PRDX6 mRNA显著增加(P〈0.05),PRDX6蛋白在不同细胞株表达水平不同,PRDX2-5 mRNA和蛋白差异均无统计学意义(P〉0.05);放线菌D组完全阻断了MG132对PRDX1 mRNA的表达上调;硼替佐米、蛋白酶体抑制剂(PSI)、乳泡素和环氧霉素组中PRDX1 mRNA和蛋白表达水平亦显著增加(P〈0.01)。结论 蛋白酶体抑制剂在转录水平上上调人甲状腺癌细胞中PRDX1基因的表达,对PRDX1mRNA的稳定性没有影响。【Objective】 To investigate the mechanism of Peroxiredoxins(PRDXs) expression in the panel of cancer cells affected by proteasome inhibitor. 【Methods】 A panel of cancer cells were selected for the investigation, set up control group and proteasome inhibitor treatment groups; the expression of PRDXs mRNA and protein in the panel of cancer cells was confirmed by real-time RT-PCR and Western blot, respectively.【Results】MG132 significantly elevated PRDX1 mRNA, protein and PRDX6 mRNA levels(P 〈0.05), Paradoxically, MG132 exposure had no stable effects on PRDX6 in the panel of thyroid cancer cells, while PRDX2-5had no obvious effects(P 〉0.05) when compared with control group; Pretreatment with the transcription inhibitor Actinomycin D completely blocked the upregulation of PRDX1 by MG132. Similar to MG132, four other proteasome inhibitors Bortezomib, PSI, Lactacystin, and Epoxomycin also elevated PRDX1 mRNA and protein expression levels in FRO cells(P 〈0.01). 【Conclusion】 Proteasome inhibitors elevated PRDX1 expression at the transcriptional level, had no effect on PRDX1 mRNA stability.
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