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目的研究β干扰素(IFN-β)和全反式维甲酸(ATRA)联合应用对Hep G2人肝癌细胞增殖和凋亡的影响,并探讨Janus激酶2/信号转导子与转录激活子3(JAK2/STAT3)通路在其中可能的机制。方法分别用1000 U/m L IFN-β、10μmol/L ATRA及1000 U/m L IFN-β联合10μmol/L ATRA处理Hep G2细胞24 h,采用MTT法检测Hep G2细胞的增殖抑制率,流式细胞术检测细胞凋亡。Western blot法检测磷酸化的Janus激酶2(p-JAK2)和磷酸化的信号转导子与转录激活子3(p-STAT3)、维甲酸-干扰素诱导死亡相关基因19(GRIM-19)、Bcl-2、Bcl-xl、Bax蛋白的表达。结果 IFN-β、ATRA作用于细胞后,Hep G2细胞增殖受到抑制,同时诱导细胞发生凋亡,IFN-β联合ATRA联合处理作用更强;Hep G2细胞中p-JAK2和p-STAT3蛋白的表达在IFN-β或ATRA作用下减弱,GRIM-19和Bax蛋白表达升高。IFN-β联合ATRA处理作用更强。结论 IFN-β联合ATRA通过抑制JAK2/STAT3信号通路抑制Hep G2人肝癌细胞的增殖并促进其凋亡。
Objective To investigate the effects of combination of interferon-β (IFN-β) and all-trans retinoic acid (ATRA) on the proliferation and apoptosis of Hep G2 human hepatocellular carcinoma cells and to explore the relationship between Janus kinase 2 / signal transducer and activator of transcription 3 JAK2 / STAT3) pathway in which possible mechanisms. Methods Hep G2 cells were treated with 1000 U / m L IFN-β, 10 μmol / L ATRA and 1000 U / m L IFN-β in combination with 10 μmol / L ATRA for 24 h. MTT assay was used to detect the proliferation inhibition rate Cytometry to detect apoptosis. The phosphorylation of Janus kinase 2 (p-JAK2), phosphorylation of signal transducers and activators of transcription 3 (p-STAT3), GRIM-19 induced death by the retinoic acid- Bcl-2, Bcl-xl, Bax protein expression. Results After treated with IFN-β and ATRA, the proliferation of Hep G2 cells was inhibited and the apoptosis of Hep G2 cells was induced. The combination of IFN-β and ATRA enhanced the expression of p-JAK2 and p-STAT3 in Hep G2 cells In IFN-β or ATRA decreased, GRIM-19 and Bax protein expression increased. IFN-β combined with ATRA treatment stronger. Conclusion IFN-β combined with ATRA can inhibit the proliferation and promote the apoptosis of Hep G2 human hepatocellular carcinoma cells by inhibiting JAK2 / STAT3 signaling pathway.