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波形蛋白基因异常的启动子甲基化可能与结直肠癌发生有关:一项荟萃分析。

Aberrant promoter methylation of the vimentin gene may contribute to colorectal carcinogenesis: a meta-analysis.

作者信息

Li Yun-Wei, Kong Fan-Min, Zhou Jian-Ping, Dong Ming

机构信息

Department of General Surgery, the First Affiliated Hospital, China Medical University, Nanjing North Street No.155, Heping District, Shenyang, 110001, People's Republic of China.

出版信息

Tumour Biol. 2014 Jul;35(7):6783-90. doi: 10.1007/s13277-014-1905-1. Epub 2014 Apr 12.

DOI:10.1007/s13277-014-1905-1
PMID:24729088
Abstract

This meta-analysis of published cohort studies was conducted to evaluate how closely the promoter methylation of the vimentin gene is correlated with the pathogenesis of colorectal carcinogenesis (CRC). The Web of Science (1945 ~ 2013), Cochrane Library Database (issue 12, 2013), PubMed (1966 ~ 2013), EMBASE (1980 ~ 2013), CINAHL (1982 ~ 2013), and Chinese Biomedical Database (CBM) (1982 ~ 2013) were searched without language restrictions. Meta-analyses were conducted using Stata software (Version 12.0, Stata Corporation, College Station, TX, USA). Odds ratios (ORs) and 95 % confidence intervals (95 %CI) were calculated. Seven clinical cohort studies with a total of 467 CRC subjects met our inclusion criteria. Our meta-analysis results demonstrated that the frequency of vimentin promoter methylation in cancer tissues was significantly higher than in normal and benign tissues (cancer tissues vs. normal tissues: OR = 32.41, 95 %CI = 21.04 ~ 49.93, P < 0.001; cancer tissues vs. benign tissues: OR = 1.60, 95 %CI 1.05 ~ 2.42, P = 0.028). Ethnicity-stratified analysis indicated that the frequency of aberrant vimentin promoter methylation was correlated with the pathogenesis of CRC in both Asians and Caucasians. The findings of our meta-analysis confirm that vimentin methylation may play a crucial role in the pathogenesis of CRC.

摘要

开展此项已发表队列研究的荟萃分析,旨在评估波形蛋白基因启动子甲基化与结直肠癌发生机制(CRC)的关联程度。检索了科学网(1945年至2013年)、考克兰图书馆数据库(2013年第12期)、PubMed(1966年至2013年)、EMBASE(1980年至2013年)、护理学与健康领域数据库(CINAHL,1982年至2013年)以及中国生物医学文献数据库(CBM,1982年至2013年),无语言限制。使用Stata软件(版本12.0,美国德克萨斯州大学城Stata公司)进行荟萃分析。计算比值比(OR)和95%置信区间(95%CI)。七项临床队列研究共纳入467例CRC受试者,符合纳入标准。我们的荟萃分析结果表明,癌组织中波形蛋白启动子甲基化频率显著高于正常组织和良性组织(癌组织与正常组织比较:OR = 32.41,95%CI = 21.04至49.93,P < 0.001;癌组织与良性组织比较:OR = 1.60,95%CI 1.05至2.42,P = 0.028)。按种族分层分析表明,亚洲人和高加索人中波形蛋白启动子异常甲基化频率均与CRC发病机制相关。我们的荟萃分析结果证实,波形蛋白甲基化可能在CRC发病机制中起关键作用。

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