目的观察人口腔鳞状细胞癌(OSCC)组织中上皮间质化相关蛋白及转录因子Twist的表达,研究Twist在OSCC上皮间质化中的作用及OSCC转移情况的相关性,并探讨其在人OSCC中的临床意义。方法通过免疫组织化学及原位杂交的方法分别检测30例OSCC组...目的观察人口腔鳞状细胞癌(OSCC)组织中上皮间质化相关蛋白及转录因子Twist的表达,研究Twist在OSCC上皮间质化中的作用及OSCC转移情况的相关性,并探讨其在人OSCC中的临床意义。方法通过免疫组织化学及原位杂交的方法分别检测30例OSCC组织中上皮源性标记物E-钙黏蛋白(E-cad)和细胞角蛋白(CK),间质源性标记物N-钙黏蛋白(N-cad),转录因子Twist蛋白及m RNA的表达情况,并与临床病理资料作对照分析。结果免疫组织化学结果:在OSCC组织中,Twist、N-cad的表达明显高于正常组织,E-cad及CK的表达明显低于正常组织(P<0.05);在OSCC中低分化组,Twist、N-cad的表达高于高分化组,E-cad及CK的表达明显低于高分化组(P<0.05);在有淋巴结转移组中,Twist、N-cad的表达高于无淋巴结转移组,E-cad及CK的表达低于无淋巴结转移组(P<0.05)。原位杂交结果:Twist m RNA在OSCC中低分化组,T3、T4组和有转移淋巴结组的表达分别高于高分化组,T1、T2组和无淋巴结转移组,以上差异均有统计学意义(P<0.05)。结论 OSCC组织中存在上皮间质化,Twist可使肿瘤细胞的侵袭力增加,促进OSCC的浸润和转移。联合检测Twist、E-cad和N-cad的表达可能会更有效地判断和预测OSCC的转移。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
缺氧是肿瘤微环境的主要特点,通过缺氧诱导因子(hypoxia-inducible factor,HIF)激活众多靶基因,从而影响肿瘤的代谢、增殖、凋亡、侵袭转移、耐药等多个方面。上皮细胞间质化(epithelial to mesenchymal transition,EMT)是肿瘤发生侵袭...缺氧是肿瘤微环境的主要特点,通过缺氧诱导因子(hypoxia-inducible factor,HIF)激活众多靶基因,从而影响肿瘤的代谢、增殖、凋亡、侵袭转移、耐药等多个方面。上皮细胞间质化(epithelial to mesenchymal transition,EMT)是肿瘤发生侵袭转移的重要起始过程,缺氧亦是EMT的诱发因素之一并可通过多条信号转导通路包括TGF-β,Notch,Wnt/β-catenin等调节EMT。研究缺氧诱导EMT的机制并阻断其进程,可成为治疗肿瘤的新靶点。展开更多
文摘目的观察人口腔鳞状细胞癌(OSCC)组织中上皮间质化相关蛋白及转录因子Twist的表达,研究Twist在OSCC上皮间质化中的作用及OSCC转移情况的相关性,并探讨其在人OSCC中的临床意义。方法通过免疫组织化学及原位杂交的方法分别检测30例OSCC组织中上皮源性标记物E-钙黏蛋白(E-cad)和细胞角蛋白(CK),间质源性标记物N-钙黏蛋白(N-cad),转录因子Twist蛋白及m RNA的表达情况,并与临床病理资料作对照分析。结果免疫组织化学结果:在OSCC组织中,Twist、N-cad的表达明显高于正常组织,E-cad及CK的表达明显低于正常组织(P<0.05);在OSCC中低分化组,Twist、N-cad的表达高于高分化组,E-cad及CK的表达明显低于高分化组(P<0.05);在有淋巴结转移组中,Twist、N-cad的表达高于无淋巴结转移组,E-cad及CK的表达低于无淋巴结转移组(P<0.05)。原位杂交结果:Twist m RNA在OSCC中低分化组,T3、T4组和有转移淋巴结组的表达分别高于高分化组,T1、T2组和无淋巴结转移组,以上差异均有统计学意义(P<0.05)。结论 OSCC组织中存在上皮间质化,Twist可使肿瘤细胞的侵袭力增加,促进OSCC的浸润和转移。联合检测Twist、E-cad和N-cad的表达可能会更有效地判断和预测OSCC的转移。
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).
文摘缺氧是肿瘤微环境的主要特点,通过缺氧诱导因子(hypoxia-inducible factor,HIF)激活众多靶基因,从而影响肿瘤的代谢、增殖、凋亡、侵袭转移、耐药等多个方面。上皮细胞间质化(epithelial to mesenchymal transition,EMT)是肿瘤发生侵袭转移的重要起始过程,缺氧亦是EMT的诱发因素之一并可通过多条信号转导通路包括TGF-β,Notch,Wnt/β-catenin等调节EMT。研究缺氧诱导EMT的机制并阻断其进程,可成为治疗肿瘤的新靶点。
