BTB/POZ结构域蛋白7假基因1在肝细胞癌中的表达及功能的初步研究

Preliminary study of expression and function of BTB/POZ domaincontaining protein 7 pseudogene 1 in hepatocellular carcinoma

目的:探讨BTB/POZ结构域蛋白7(BTBD7)假基因1(BTBD7P1)在肝细胞癌(HCC)中的表达及功能。方法:检测106例配对的HCC组织与癌旁组织标本中BTBD7P1 m RNA的表达,分析BTBD7P1m RNA表达与HCC患者临床病理特征及预后的关系。用BTBD7P1过表达慢病毒载体转染HCC细胞系Bel7404后,检测细胞增殖率以及BTBD7 m RNA与蛋白的表达。结果:HCC组织中BTBD7P1相对表达量明显低于癌旁组织为(0.71 vs.2.14,P<0.05);BTBD7P1m RNA低表达与肿瘤大小、卫星灶、分化程度、静脉血管侵犯、出血坏死、HCC分期明显有关(均P<0.05);BTBD7P1 m RNA低表达患者的1、3、5年总体生存率及无瘤生存率均明显低于BTBD7P1m RNA高表达患者(均P<0.05)。与转染空载体质粒的对照组Bel7404细胞比较,转染BTBD7P1过表达慢病毒载体的Bel7404细胞,细胞增殖能力明显减低,BTBD7 m RNA表达明显下调(均P<0.05),但BTBD7蛋白表达无明显变化(P>0.05)。结论:BTBD7P1可能在m RNA水平对亲本基因BTBD7表达进行调控,从而参与了HCC发生与发展。

Objective： To investigate the expression of BTB/POZ domain-containing protein 7 （BTBD7） pseudogene 1 （BTBD7P 1） in hepatocellular carcinoma （HCC） and its action. Methods： The BTBD7P1 mRNA expressions in 106 paired specimens of HCC tissue and its adjacent tissue were determined, and the relations of BTBD7P1 mRNA expression with the clinicopathologic features and prognosis of the HCC patients were analyzed. In HCC Be17404 cells after transfected with BTBD7P1 overexpression lentiviral vectors, the proliferation and expressions ofBTBD7 mRNA and protein were measured. Results： The relative expression level of BTBD7P 1 mRNA in HCC tissue was significantly lower than that in ad）acent tissue （0.71 vs. 2.14, P〈0.05）; lower expression of BTBDTP 1 was significantly associated with tumor size, satellite lesions, degree of differentiation, vascular invasion, hemorrhagic necrosis, and stage of HCC （all P〈0.05）; the 1-, 3- and S-year overall and tumor-free survival rates in patients with low BTBD7P1 mRNA expression were significantly lower than those in patients with higher BTBDTP1 mRNA expression （both P〈0.05）. In Be17404 cells transfected with BTBD7P 1 overexpression lentiviral vectors, the cell proliferation was significantly decreased and the BTBD7 mRNA expression was significantly down-regulated （both P〈0.0S）, but BTBD7 protein expression showed no significant change （P〉0.05） compared with control Be17404 cells transfected with empty vectors. Conclusion： BTBD7P1 may probably regulate the expression of its parental gene BTBD7 at mRNA level and thereby participate in the occurrence and development of HCC.