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基因沉默伴侣蛋白CCT6A对甲状腺未分化癌细胞增殖和侵袭能力的影响

Effects of chaperone protein CCT6A on proliferation and invasion in anaplastic thyroid cancer
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摘要 目的:探讨基因沉默伴侣蛋白CCT6A对甲状腺未分化癌细胞(8505C和CAL-62)增殖和侵袭能力的影响。方法:比较人新鲜甲状腺癌癌旁组织、甲状腺乳头状癌组织、甲状腺未分化癌组织中CCT6A mRNA相对表达量;选择两种人甲状腺未分化癌细胞株8505C和CAL-62,构建敲低CCT6A蛋白表达水平的细胞系,利用蛋白质印迹法验证转染效率后检测信号转导蛋白SMAD2的表达和活化。CCK8实验检测敲低CCT6A表达后甲状腺未分化癌细胞增殖能力的变化,Transwell实验检测细胞的迁移能力。结果:甲状腺未分化癌组织中CCT6A的mRNA表达水平上调。敲低CCT6A的甲状腺未分化癌细胞8505C和CAL-62中信号转导蛋白SMAD2的磷酸化激活水平显著下调。与阴性对照组相比,基因沉默实验组的细胞增殖能力显著下降,其侵袭能力亦显著减弱(P<0.05)。结论:CCT6A在甲状腺未分化癌发生发展中起关键作用,敲低CCT6A可通过下调SMAD2活化水平抑制细胞增殖和侵袭能力,未来CCT6A可能成为治疗甲状腺未分化癌的潜在靶点。 Objective:To investigate the effects of CCT6 A on proliferation and invasion of anaplastic thyroid cancer cells(8505 C and CAL-62).Methods:Fresh human paracancerous tissue,papillary thyroid cancer tissue and anaplastic thyroid cancer tissue was collected to measure the relative expression of CCT6 A mRNA.Two anaplastic thyroid cancer cell lines(8505 C and CAL-62)were transfected to knockdown CCT6 A protein expression.The transfection efficiency was verified by Western blot,the expression and phosphorylation activation of signaltransduction protein SMAD2 were detected.CCK8 assay was performed to detect proliferation ability of anaplastic thyroid cancer cells after CCT6 A downregulation,and transwell assay was used to detect the migration ability of8505 C and CAL-62 cells.Results:Compared with paracancerous tissues and papillary thyroid carcinoma tissues,the expression of CCT6 A mRNA in anaplastic thyroid cancer tissues was significantly higher.The phosphorylation and activation of signal transduction protein SMAD2 were significantly downregulated in 8505 C and CAL-62 cells with CCT6 A knockdown.Compared with the negative control group,the proliferation and invasion ability of cells in sh-CCT6 A group were significantly decreased(P<0.05).Conclusion:CCT6 A plays a key role in the development and progression of anaplastic thyroid cancer.CCT6 A knockdown can inhibit cell proliferation and invasion by suppressing the activation level of SMAD2.CCT6 A may become a potential target for anaplastic thyroid cancer therapy.
作者 孙骥 崔文娟 李敬东 唐涛 SUN Ji;CUI Wenjuan;LI Jingdong;TANG Tao(Department of Hepatobiliary Surgery,Affliated Hospital of North Sichuan Medical College,Nanchong 637000,China;Hepatobiliary,Pancreatic and Intestinal Diseases Research Institute of North Sichuan Medical College,Nanchong 637000,China;The Third Department of Neurology,Suining Central Hospital,Suining 629000,China)
出处 《现代医学》 2021年第7期719-724,共6页 Modern Medical Journal
基金 四川省科技计划项目(2019YJ0384) 南充市科技战略合作项目(NSMC20170413) 南充市市校科技战略合作项目(18SXHZ0305) 四川省医学科研青年创新课题(Q20024)
关键词 分子伴侣蛋白 CCT6A 甲状腺未分化癌 SMAD2 细胞增殖 细胞侵袭 molecular chaperone protein CCT6A anaplastic thyroid cancer SMAD2 cell proliferation cell invasion
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