前S2区突变LHBs与C53蛋白相互作用对HepG2细胞生物学功能的影响

Study on the effects on cell biology functions of HepG2 cell line by interaction between LHBs and C53

目的明确肝癌细胞系HepG2中前S2区突变乙型肝炎表面抗原大蛋白（hepatitis Bvirus large surface protein，LHBs）与C53蛋白相互作用对细胞生物学功能的影响。方法分别构建pc—MV-5a·pres2LHBs和pCDNA-4-C53质粒，共同转染肝癌细胞系HepG2后，分别检测其相互作用对Chkl活性的影响；BrdU法细胞增殖检测明确其对细胞有丝分裂及增殖的影响。结果成功构建pc—MV-5a—pres2LHBs和pCDNA-4-C53质粒；其在细胞内的相互作用增加细胞Cdkl活性并促进细胞的增殖和有丝分裂过程。结论肝癌细胞系HepG2内pres2LHBs及C53的相互作用对细胞生物学功能存在影响，提示可能与HBV后肝癌的发病机制相关。

Objective To identify the effects on cell biology functions of HepG2 cells by interaction between pre-S2 LHBs and C53. Methods The plasmids pCMV-5a- pre-S2 LHBs and pCDNA-4-C53 were reconstructed. The plasmids pCMV-Sa-LHBs and pCDNA-4-C53 were cotransfected into the hepatoma cell line HepG2, the roles of the binding of pre-S2 LHBs with C53 on Cdkl, Chkl activation and mitotic entry were studied. Results The plasmids pCMV-Sa-LHBs and pCDNA-4-CSB were reconstructed successfully. The binding of pre $2 LHBs with C53 increased Cdkl activation and mitotic entry. Conclusions By coun- teracting C53, pre-S2 LHBs promotes Cdkl activation and mitotic entry in both unperturbed cell cycle pro- gression and delayed the function of Chkl, which may be a novel potential mechanism for HBV-induced hep- atocellular carcinoma （HCC）.