骨形成蛋白-2通过JNK信号通路促进肝癌HepG2细胞凋亡

BMP-2 Induces Apoptosis of Human Hepatocellular Carcinoma Cell HepG2 via JNK Signaling Pathway

目的观察骨形成蛋白-2(bone morphogenetic protein-2,BMP-2)对人肝癌HepG-2细胞凋亡的作用及其信号通路机制。方法用流式细胞分析和细胞凋亡ELISA法检测HepG2细胞凋亡,用Western blot法检测丝裂原激活蛋白激酶(MAPKs)和磷脂酰肌醇3-激酶(PI3K)下游效应因子Akt的激活,采用信号通路阻断剂预处理HepG2细胞观察BMP-2影响细胞凋亡的机制。结果BMP-2诱导HepG2细胞凋亡,呈时间和剂量依赖性;BMP-2激活HepG2细胞JNK激酶,但不能激活ERK1/2、p38及Akt;采用JNK信号通路抑制剂SP600125可阻断BMP-2对HepG-2细胞JNK的激活,并消除BMP-2对HepG-2细胞凋亡的作用。结论BMP-2通过JNK信号通路途径诱导HepG2肝癌细胞凋亡。

Objective To characterize the effect of BMP- 2 on apoptosis of human hepatocellular carcinoma cell HepG2 and the signaling pathway involved in it. Methods Cell apoptosis was assessed by flow cytometry and ELISA. Western blot was used to show the activation of MAPKs （ERK1/2, JNK and p38） and Akt. A specific JNK inhibitor SP600125 was used for the signaling pathway study. Results BMP - 2 dose - and time - dependent effects induced HepG2 cells apoptosis. BMP - 2 induced JNK activation in HepG2 cells. SP600125 abolished the effects of BMP - 2 on JNK activation and apoptosis in HepG2 cells. Conclusions The present study suggests that BMP- 2 induces HepG2 cells apoptosis through JNK signaling pathway.