TGF-β1诱导人肝癌细胞HepG2上皮间质转化及对JAK-STAT3信号通路的影响

摘要

Objective To investigate the effect of TGF-β1 on epithelial-mesenchymal transition and JAK-STAT3 ex-pression in HepG2 cells. Methods HepG2 cells were incubated with 5μg·mL-1 TGF-β1. Cell morphologic changes were observed by microscope. The mRNA expression of E-cadherin and Vimentin were examined by real time-PCR and the pro-tein expressions of E-cadherin, Vimentin, JAK, p-JAK, STAT3, p-STAT3 were detected by western blot. Results TGF-β1 activated the JAK-STAT3 signaling and increased the Vimentin expression. Meanwhile, it decreased the E-cadherin ex-pression and significantly induced EMT in HepG2 cells. Conclusion TGF-β1 could induce EMT in HepG2 cells, and this may be involved with the stimulation of JAK-STAT3 signaling.%目的：探讨TGF-β1诱导人肝癌细胞HepG2上皮间质转化及对JAK-STAT3表达的影响。方法采用5μg·mL-1 TGF-β1处理人肝癌细胞HepG2细胞，用倒置显微镜观察细胞形态变化，用Real time-PCR检测E-cadherin和Vimentin的mRNA表达变化；Western blot检测E-cadherin、Vimentin、JAK、p-JAK、STAT3及p-STAT3的蛋白表达变化。结果 TGF-β1可激活JAK-STAT3通路，上调Vimentin表达，同时下调E-cadherin的表达，并显著促进其上皮间质转化。结论 TGF-β1可以诱导人肝癌细胞HepG2上皮间质转化，其机制可能与JAK-STAT3信号通路激活有关。