目的探讨程序性死亡因子配体-1(programmed death ligand-1,PD-L1)表达、上皮-间质细胞转化(epithelial-mesenchymal transition,EMT)发生与卵巢癌临床病理特征的关系及两者的相关性。方法采用免疫组化SP法染色,并检测106例原发性卵巢...目的探讨程序性死亡因子配体-1(programmed death ligand-1,PD-L1)表达、上皮-间质细胞转化(epithelial-mesenchymal transition,EMT)发生与卵巢癌临床病理特征的关系及两者的相关性。方法采用免疫组化SP法染色,并检测106例原发性卵巢上皮性癌、40例良性上皮性肿瘤组织中PD-L1和EMT相关蛋白(E-cadherin、vimentin)的表达,分析人卵巢癌组织中PD-L1表达与EMT发生之间的关系。结果 106例卵巢癌组织中PD-L1的阳性率为65.1%(69/106),E-cadherin的阳性率为58.5%(62/106),vimentin的阳性率为53.8%(57/106),EMT发生率为35.8%(38/106)。在有淋巴结转移组、有脉管侵犯组及有恶性腹水组中PD-L1表达及EMT发生率均高于无淋巴结转移组、无脉管侵犯组及无恶性腹水组,其差异均有统计学意义(P<0.05)。69例PD-L1阳性卵巢癌组织中有34例EMT表型,PD-L1阳性与EMT表型之间呈明显的正相关(r=0.300,P=0.002)。结论在人卵巢癌组织中,PD-L1表达与EMT相关蛋白的表达有密切关系,两者可能在卵巢癌的发生、发展过程中发挥协调作用。展开更多
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
文摘目的探讨程序性死亡因子配体-1(programmed death ligand-1,PD-L1)表达、上皮-间质细胞转化(epithelial-mesenchymal transition,EMT)发生与卵巢癌临床病理特征的关系及两者的相关性。方法采用免疫组化SP法染色,并检测106例原发性卵巢上皮性癌、40例良性上皮性肿瘤组织中PD-L1和EMT相关蛋白(E-cadherin、vimentin)的表达,分析人卵巢癌组织中PD-L1表达与EMT发生之间的关系。结果 106例卵巢癌组织中PD-L1的阳性率为65.1%(69/106),E-cadherin的阳性率为58.5%(62/106),vimentin的阳性率为53.8%(57/106),EMT发生率为35.8%(38/106)。在有淋巴结转移组、有脉管侵犯组及有恶性腹水组中PD-L1表达及EMT发生率均高于无淋巴结转移组、无脉管侵犯组及无恶性腹水组,其差异均有统计学意义(P<0.05)。69例PD-L1阳性卵巢癌组织中有34例EMT表型,PD-L1阳性与EMT表型之间呈明显的正相关(r=0.300,P=0.002)。结论在人卵巢癌组织中,PD-L1表达与EMT相关蛋白的表达有密切关系,两者可能在卵巢癌的发生、发展过程中发挥协调作用。
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).
