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作 者:赵娜[1] 王琛 郑琴 张鑫达 刘洋[1] ZHAO Na;WANG Chen;ZHENG Qin;ZHANG Xin-da;LIU Yang(Department of Pathology,China Medical University,Shenyang 110122,China)
机构地区:[1]中国医科大学基础医学院病理学教研室,辽宁沈阳110122
出 处:《解剖科学进展》2022年第2期224-228,共5页Progress of Anatomical Sciences
基 金:辽宁省教育厅科学研究经费(JC2019027)。
摘 要:目的 研究CCDC106通过降解野生型p53促进MCF-7和Hela细胞增殖、集落形成和侵袭的能力。方法 通过免疫荧光观察CCDC106在MCF-7和Hela细胞中的亚定位。采用CCK8、集落和Transwell实验,解析CCDC106对其功能学的影响,并通过Western blot检测CCDC106对下游周期蛋白和EMT相关蛋白的影响,并进一步通过免疫荧光共定位和免疫共沉证实CCDC106和p53关系。结果 转染CCDC106促进MCF7和Hela细胞的增殖、集落形成和侵袭能力,而特异性干扰CCDC106抑制MCF-7和Hela细胞的增殖、集落形成和侵袭能力。相关的下游周期蛋白和EMT相关蛋白也得到相一致的结果。CCDC106和p53有共定位且能相互结合。结论 CCDC106通过降解野生型p53促进MCF-7和Hela细胞的增殖和侵袭,是潜在治疗靶点。Objective To study the effect of CCDC106 on the proliferation, colony formation and invasion of MCF-7 and Hela cells by degrading wild-type p53. Methods CCDC106 subcellular distribution in MCF-7 and Hela cell lines was evaluated by immunofluorescence. The effects of CCDC106 on its functionology were analyzed by CCK8, colony and Transwell experiments, and the effects of CCDC106 on downstream cyclins and EMT-related proteins were detected by Western blot. The relationship between CCDC106 and p53 was further confirmed by immunofluorescence co-localization and immunoprecipitation. Results The transfection of CCDC106 promoted the proliferation,colony formation and invasion of MCF-7 and Hela cells, while interfering with CCDC106 inhibited cell proliferation, colony formation and invasion of MCF-7 and Hela cells. The results of Western blot were also consistent with those of downstream cyclins and EMT-related proteins. CCDC106 and p53 had co-localization and could bind to each other. Conclusion CCDC106promotes the proliferation and invasion of MCF-7 and Hela cells via degrading wild-type p53, which would provide a potential therapeutic target and basis for targeted therapy of tumor.
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