文章摘要

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

作者: 1陶一明, 1胡宽, 2汤参娥, 1冯铁诚, 1王志明
1 中南大学湘雅医院 肝脏外科，湖南 长沙 410008
2 中南大学湘雅医院医学科学研究中心，湖南 长沙 410008
通讯: 王志明 Email: wzmxycsu@hotmail.com
DOI: 10.3978/.10.3978/j.issn.1005-6947.2017.01.007
基金: 国家自然科学基金资助项目, 81372630 湖南自然科学基金资助项目, 12JJ3118 湖南省科学技术厅科技计划资助项目, 2013FJ4112 “湘雅医院——北大末名临床与康复研究基金”资助项目, xywm2015126

摘要

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 mRNA的表达，分析BTBD7P1 mRNA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 mRNA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）；BTBD7P1 mRNA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 mRNA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BTBD7P1 mRNA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 mRNA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mRNA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。
关键词： 癌，肝细胞 BTB/POZ结构域蛋白7 拟基因 RNA，长链非编码

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

Authors: 1TAO Yiming, 1HU Kuan, 2TANG Can'e, 1FENG Tiecheng, 1WANG Zhiming
1 Department of Liver Surgery, Xiangya Hospital, Central South University, Changsha 410008, China
2 Research Institute of Medical Sciences, Xiangya Hospital, Central South University, Changsha 410008, China

CorrespondingAuthor:WANG Zhiming Email: wzmxycsu@hotmail.com

Abstract

Objective: To investigate the expression of BTB/POZ domain-containing protein 7 (BTBD7) pseudogene 1 (BTBD7P1) 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 Bel7404 cells after transfected with BTBD7P1 overexpression lentiviral vectors, the proliferation and expressions of BTBD7 mRNA and protein were measured. Results: The relative expression level of BTBD7P1 mRNA in HCC tissue was significantly lower than that in adjacent tissue (0.71 vs. 2.14, P<0.05); lower expression of BTBD7P1 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 5-year overall and tumor-free survival rates in patients with low BTBD7P1 mRNA expression were significantly lower than those in patients with higher BTBD7P1 mRNA expression (both P<0.05). In Bel7404 cells transfected with BTBD7P1 overexpression lentiviral vectors, the cell proliferation was significantly decreased and the BTBD7 mRNA expression was significantly down-regulated (both P<0.05), but BTBD7 protein expression showed no significant change (P>0.05) compared with control Bel7404 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.
Keywords：