Objective To investigate the expression of cyclin-dependent kinase 8(CDK8)in esophageal squamous cell carcinoma(ESCC)and its effect on ESCC cells,and to explore its potential molecular mechanism.Methods The expression...Objective To investigate the expression of cyclin-dependent kinase 8(CDK8)in esophageal squamous cell carcinoma(ESCC)and its effect on ESCC cells,and to explore its potential molecular mechanism.Methods The expression level of CDK8 mRNA was analyzed using UALCAN database,and then the expression level of CDK8 protein in tumor tissues of ESCC patients was detected by immunohistochemistry(IHC).Esophageal cancer cell lines Kyse-30 and Kyse-150 were stably transfected with lentivirus to achieve knockdown and overexpression of CDK8.EdU proliferation assay,cell colony formation assay,cell cycle assay,cell scratch assay and invasion assay were used to explore the effect of CDK8 protein expression level on the phenotype of ESCC cells.Subsequently,the effect of CDK8 on the growth of esophageal cancer xenografts in vitro was observed by subcutaneous tumor formation assay in mice.Finally,the expression of proliferation and metastasis related proteins was detected by Western blot.Results CDK8 showed high transcription and protein expression levels in ESCC tissues compared with normal esophageal tissues.Knockdown of CDK8 expression significantly inhibited the proliferation,migration and invasion of ESCC cells.In addition,inhibition of CDK8 expression significantly affected the JAK2/STAT3 pathway and the expression of E-cadherin/N-cadherin,while overexpression of CDK8 reversed these effects.Inhibition of STAT3 pathway reversed the promoting effect of CDK8 overexpression on ESCC cell phenotype.Conclusion CDK8 is a cancer-promoting factor of ESCC,which mediates the phosphorylation of JAK2/STAT3 and epithelial-mesenchymal transition(EMT).展开更多
慢性乙型肝炎病毒（Hepatitis B virus,HBV）感染是世界范围内最常见的慢性病毒性感染,全球约有20亿人口有血清学证据证实现症或既往感染HBV,其中约3.5亿人口罹患慢性HBV感染[1,2];慢性HBV感染可致慢性肝病,与肝硬化、肝癌的发生密切相...慢性乙型肝炎病毒（Hepatitis B virus,HBV）感染是世界范围内最常见的慢性病毒性感染,全球约有20亿人口有血清学证据证实现症或既往感染HBV,其中约3.5亿人口罹患慢性HBV感染[1,2];慢性HBV感染可致慢性肝病,与肝硬化、肝癌的发生密切相关,在2010年全球疾病负担研究中,HBV感染位居首位,在导致死亡的病因中位列第10（78.6万/年）[3],基于这些数据,展开更多
文摘Objective To investigate the expression of cyclin-dependent kinase 8(CDK8)in esophageal squamous cell carcinoma(ESCC)and its effect on ESCC cells,and to explore its potential molecular mechanism.Methods The expression level of CDK8 mRNA was analyzed using UALCAN database,and then the expression level of CDK8 protein in tumor tissues of ESCC patients was detected by immunohistochemistry(IHC).Esophageal cancer cell lines Kyse-30 and Kyse-150 were stably transfected with lentivirus to achieve knockdown and overexpression of CDK8.EdU proliferation assay,cell colony formation assay,cell cycle assay,cell scratch assay and invasion assay were used to explore the effect of CDK8 protein expression level on the phenotype of ESCC cells.Subsequently,the effect of CDK8 on the growth of esophageal cancer xenografts in vitro was observed by subcutaneous tumor formation assay in mice.Finally,the expression of proliferation and metastasis related proteins was detected by Western blot.Results CDK8 showed high transcription and protein expression levels in ESCC tissues compared with normal esophageal tissues.Knockdown of CDK8 expression significantly inhibited the proliferation,migration and invasion of ESCC cells.In addition,inhibition of CDK8 expression significantly affected the JAK2/STAT3 pathway and the expression of E-cadherin/N-cadherin,while overexpression of CDK8 reversed these effects.Inhibition of STAT3 pathway reversed the promoting effect of CDK8 overexpression on ESCC cell phenotype.Conclusion CDK8 is a cancer-promoting factor of ESCC,which mediates the phosphorylation of JAK2/STAT3 and epithelial-mesenchymal transition(EMT).
文摘慢性乙型肝炎病毒（Hepatitis B virus,HBV）感染是世界范围内最常见的慢性病毒性感染,全球约有20亿人口有血清学证据证实现症或既往感染HBV,其中约3.5亿人口罹患慢性HBV感染[1,2];慢性HBV感染可致慢性肝病,与肝硬化、肝癌的发生密切相关,在2010年全球疾病负担研究中,HBV感染位居首位,在导致死亡的病因中位列第10（78.6万/年）[3],基于这些数据,
