Article Summary
耿西林,张 静,李 晖,杨宇宇,张 煜,常虎林.线粒体E3泛素连接酶MARCH5表达上调促进肝癌生长[J].现代生物医学进展英文版,2021,(3):424-428.
线粒体E3泛素连接酶MARCH5表达上调促进肝癌生长
Over-expression of MARCH5 Promotes Tumor Growth in Liver Cancer
Received:May 28, 2020  Revised:June 24, 2020
DOI:10.13241/j.cnki.pmb.2021.03.005
中文关键词: MARCH5  线粒体  增殖  克隆形成  肝癌
英文关键词: MARCH5  Mitochondrial  Proliferation  Colony formation  Liver cancer
基金项目:陕西省自然科学基金青年项目(2020JQ-948)
Author NameAffiliationE-mail
耿西林 陕西省人民医院肝胆外科 陕西 西安 710068 gengxilin001@163.com 
张 静 陕西省人民医院肝胆外科 陕西 西安 710068  
李 晖 陕西省人民医院肝胆外科 陕西 西安 710068  
杨宇宇 通用环球西安西航医院外一科 陕西 西安 710021  
张 煜 陕西省人民医院肝胆外科 陕西 西安 710068  
常虎林 陕西省人民医院肝胆外科 陕西 西安 710068  
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中文摘要:
      摘要 目的:膜相关锌指蛋白MARCH5(membrane-associated RING-CH 5)是定位于线粒体外膜的E3泛素连接酶,在调控线粒体分裂融合相关蛋白的表达中发挥重要作用。以往研究在多种肿瘤中证实了线粒体分裂融合的异常,但目前MARCH5在肝癌中的表达与生物学作用均不清楚。本研究旨在探讨MARCH5在肝癌组织与细胞系中的表达及其在肿瘤生长中的调控作用。方法:1).利用免疫组化实验检测62对肝癌癌与癌旁组织中MARCH5表达,以明确MARCH5在肝癌中的表达是否发生了异常改变。2). 利用qRT-PCR与Western blot实验检测4株肝癌细胞(SNU-354、SNU-368、HLE与HLF)与1株正常肝细胞HL7702中MARCH5表达,进一步分析MARCH5在肝癌细胞系中的表达改变。3). 下调肝癌细胞中MARCH5表达后,利用EDU实验与克隆形成实验分析对肝癌细胞增殖与克隆形成能力的影响。结果:1).MARCH5在肝癌组织中表达显著高于癌旁组织。2). MARCH5在4株肝癌细胞中的表达均显著高于正常肝细胞。3).下调MARCH5表达可显著抑制肝癌细胞的增殖与克隆形成。结论: MARCH5在肝癌中表达显著上调并通过诱导增殖与克隆形成而促进肝癌的生长。
英文摘要:
      ABSTRACT Objective: MARCH5 (membrane-associated RING-CH 5) is an E3 ubiqutin-protein that localized in mitochondrial membrane and functions as a regulator of mitochondrial morphology. Previous studies have indicated the close link between mitochondrial dynamic dysfunction and cancer. However, the expression and biological functions of MARCH5 in liver cancer remains unclear. The present study aims to explore the expression and tumor growth promotive role of MARCH5 in liver cancer. Methods: 1. Immunohistochemistry analysis was applied to evaluate the expression of MARCH5 in 62-paired tumor and peritumor tissues of liver cancer. 2. MARCH5 expression was further evaluated in four human liver cancer cell lines (SNU-354, SNU-368, HLE and HLF) and one normal liver cell line HL-7702. 3. The effects of MARCH5 knockdown on the proliferation and colony formation were determined by EDU (5-Ethynyl-2'- deoxyuridine) and colony formation assays in liver cancer SNU-368 cells. Results: 1. MARCH5 expression was significantly increased in tumor tissues of liver cancer when compared with peritumor tissues (P<0.001). 2. MARCH5 expression was significantly higher in four liver cancer cell lines than in normal liver cancer cell. 3. MARCH5 knockdown suppressed both proliferation and colony formation in liver cancer cells. Conclusion: MARCH5 over-expression promotes liver cancer growth through increasing cell proliferation and colony formation.
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