羧基末端结合蛋白1对肝癌细胞HepG2增殖的影响

目的 研究羧基末端结合蛋白1（C-terminal binding protein1,CtBP1）对人肝癌细胞HepG2增殖的影响及机制。 方法 采用CtBP1 siRNA转染HepG2细胞，实验分为4个组：空白对照组、转染试剂对照组、阴性序列对照组与干扰组。于转染后不同的时间收集细胞，用MTT法检测细胞增殖、流式细胞术检测细胞周期及凋亡情况。结果 CtBP1 siRNA转染有效抑制了HepG2细胞中CtBP1蛋白表达，与空白对照组比较，转染后72 h后，CtBP1蛋白下调了57.80%。 CtBP1沉默后细胞生长受到抑制（P＜0.05），转染后24、48、72、96 h生长抑制率分别为22.34%、52.15%、53.97%和54.77%；而对细胞周期分布无明显影响（P＞0.05）； 但CtBP1表达下调有促凋亡作用，与对照组相比，干扰组的细胞凋亡率显著升高（P＜0.05）。结论 CtBP1沉默能抑制HepG2细胞增殖，其机制是通过促凋亡来实现的。CtBP1能促进肿瘤生长和抑制凋亡，是潜在的肿瘤治疗靶点。

Impact of C-terminal Binding Protein 1 on Cell Proliferation of Hepatocellular Carcinoma Cell HepG2

Obiective To investigate the impaction of C-terminal binding protein 1 (CtBP1) on proliferationof hepatocellular carcinoma cell HepG2 and related mechanism.Methods siRNA targeting for CtBP1 wereintroduced into HepG2 cells to knock down CtBP1,3 control groups including blank control, transfectionreagent and control siRNA were used as controls.At different time points after transfection, HepG2 cells werecollected for MMT assay to detect cell proliferation and fl owcytometry to detect cell cycle distribution andapoptosis.Results CtBP1 siRNA effectively knocked down CtBP1 in HepG2 cell. Compared with controlgroup, CtBP1 protein signifi cantly was decreased by 57.80%.Cell growth were signifi cantly inhibited afterCtBP1 knockdown (P＜0.05). The inhibition rates of cell growth were 22.34%,52.15%,53.97% and 54.77%at 24, 48, 72 and 96 h respectively. The distribution of cell cycle was not changed but apopotic cells wereincreased significantly compared with control group.Conclusion CtBP1 knockdown could inhibit cellproliferation of HepG2 mainly through apoptosis instead of cell cycle arrest. CtBP1 is involved in cell growthand apoptosis inhibition of tumor cells, and could be a candidate for cancer targeted therapy.