目的:观察肝癥口服液含药人血清对SMMC-7721肝癌细胞TGFβ1/Sm ads信号转导通路中TGFβ受体(TGFβR)的影响。方法:以健康志愿者和肝癌患者用药前后血清培养人SMMC-7721肝癌细胞,应用RT-PCR和W estern B lotting技术观察含药血清对肝癌细...目的:观察肝癥口服液含药人血清对SMMC-7721肝癌细胞TGFβ1/Sm ads信号转导通路中TGFβ受体(TGFβR)的影响。方法:以健康志愿者和肝癌患者用药前后血清培养人SMMC-7721肝癌细胞,应用RT-PCR和W estern B lotting技术观察含药血清对肝癌细胞TGFβRⅠ和TGFβRⅡmRNA和蛋白表达的影响。结果:健康志愿者服用肝癥口服液前后血清对SMMC-7721细胞的TGFβRⅠ和TGFβRⅡ蛋白和mRNA表达无显著影响;肝癌患者肝癥口服液的含药血清可使明显受到抑制的TGFβRⅠ和TGFβRⅡ表达恢复,尤其以TGFβRⅡ表达显著上调。结论:肝癌患者肝癥口服液含药血清可增加肝癌细胞TGFβR的表达,使受到抑制的TGFβ1/Sm ads信号转导通路功能恢复。展开更多
Transforming growth factor β （TGFβ） controls cellular behavior in embryonic and adult tissues. TGFβ binding to serine/threonine kinase receptors on the plasma membrane activates Smad molecules and additional sign...Transforming growth factor β （TGFβ） controls cellular behavior in embryonic and adult tissues. TGFβ binding to serine/threonine kinase receptors on the plasma membrane activates Smad molecules and additional signaling proteins that together regulate gene expression. In this review, mechanisms and models that aim at explaining the coordination between several components of the signaling network downstream of TGFβ are presented. We discuss how the activity and duration of TGFβ receptor/Smad signaling can be regulated by post-translational modifications that affect the stability of key proteins in the pathway. We highlight finks between these mechanisms and human diseases, such as tissue fibrosis and cancer.展开更多
文摘Transforming growth factor β （TGFβ） controls cellular behavior in embryonic and adult tissues. TGFβ binding to serine/threonine kinase receptors on the plasma membrane activates Smad molecules and additional signaling proteins that together regulate gene expression. In this review, mechanisms and models that aim at explaining the coordination between several components of the signaling network downstream of TGFβ are presented. We discuss how the activity and duration of TGFβ receptor/Smad signaling can be regulated by post-translational modifications that affect the stability of key proteins in the pathway. We highlight finks between these mechanisms and human diseases, such as tissue fibrosis and cancer.
