Xie Bin, Tang Chun, Chen Ping, Gou Yuan-bin, Yuan Tao, Jin Shi-long, Zhou Yu-yang
Department of Hepatobiliary Surgery, Daping Hospital and the Field Surgery Research Institute, Third Military Medical University, Chongqing 400042, China.
Zhonghua Gan Zang Bing Za Zhi. 2009 Jul;17(7):531-4.
To explore the signal pathway mediating the regulatory effect of Hepatitis B virus X protein (HBX) on c-met gene promoter in HepG2 cells.
The expression of c-met in HBX-transfected HepG2 cells treated with different signal pathway inhibitors was detected by western blot, the invasion capability of cells was determined by Matrigel invasion assay.
ERK inhibitor U0126 inhibited the expression of the c-Met in HBx-transfected HepG2 cells. However, both p38MAPK inhibitor SB203580 and PI-3K inhibitor wortmanin had no effect on expression of the c-Met in HBx-transfected HepG2 cells. Furthermore, the ERK inhibitor U0126 also inhibited the invasiveness of HBX-transfected HepG2 cells.
HBx induces invasion of HCC via activation of ERK pathway.
探讨乙肝病毒X蛋白(HBX)对HepG2细胞中c-met基因启动子调控作用的信号转导途径。
采用蛋白质免疫印迹法检测用不同信号转导途径抑制剂处理的转染HBX的HepG2细胞中c-met的表达,用基质胶侵袭实验检测细胞的侵袭能力。
ERK抑制剂U0126抑制转染HBx的HepG2细胞中c-Met的表达。然而,p38丝裂原活化蛋白激酶抑制剂SB203580和磷脂酰肌醇-3激酶抑制剂渥曼青霉素对转染HBx的HepG2细胞中c-Met的表达均无影响。此外,ERK抑制剂U0126也抑制转染HBX的HepG2细胞的侵袭能力。
HBx通过激活ERK途径诱导肝癌细胞侵袭。