Background and objective: The CpG island aberrant promoter methylation in the tumor suppressor gene region plays an important role in the process of tumorigenesis. Relevant evidence shows that the promoter methylation of RAS association domain family 1A (RASSF1A) gene, a tumor suppressor gene, has a close relationship with non-small cell lung cancer (NSCLC) development; therefore, RASSF1A may be a potential NSCLC biomarker. This paper discussed and summarized the relationship between RASSF1A gene promoter methylation frequency and NSCLC through meta-analysis.
Methods: By searching Medline, EMBASE, CNKI, and Wanfang database, we selected and collected the published articles regarding RASSF1A gene promoter methylation and NSCLC risk according to the marked inclusion and exclusion criteria. Through meta-analysis, combined odds ratio (OR) and 95% confidence interval (CI) data were used to analyze the RASSF1A gene promoter methylation and NSCLC relationship.
Results: A total of 23 articles were utilized in this study. Results indicated that the RASSF1A gene promoter methylation rate was 41.50% (95%CI: 34%-49%) in NSCLC tissue and was 5.58% (95%CI: 2%-9%) for the control group. Compared with normal lung tissue, RASSF1A methylation frequency in tumor tissue was significantly higher than that of the control group (OR=8.72, 95%CI: 4.88-15.58, P<0.05). Subgroup analysis showed that the RASSF1A gene promoter methylation rate of tumor tissue was higher than that of plasma group (OR=10.99, 95%CI: 2.48-48.68) and normal control tissue group (OR=8.74, 95%CI: 4.39-17.41).
Conclusions: The rate of RASSF1A promoter gene methylation in NSCLC patient tissue samples was higher than that of normal lung samples, whereas the rate of RASSF1A promoter gene methylation in the tissue has more significant effect on lung cancer occurrence. This finding indicates that RASSF1A gene promoter methylation could be used as an NSCLC biomarker and was involved in NSCLC carcinogenic effects.
背景与目的 肿瘤发生、发展过程中，抑癌基因启动子区域CpG岛异常甲基化起着重要的作用。已有研究显示RAS相关区域家族1A（Ras association domain family 1A, RASSF1A）基因，作为一个抑癌基因其启动子区域甲基化与非小细胞肺癌（non-small cell lung cancer, NSCLC）的发生发展密切相关。在NSCLC患者癌组织中RASSF1A基因启动子往往表现为异常高甲基化。本研究采用meta分析的方法探讨RASSF1A基因启动子甲基化与NSCLC发生之间的关系。方法 通过检索Medline、EMBASE、CNKI和万方数据库，按照已拟定的纳入与剔除标准筛选收集公开发表的关于RASSF1A基因启动子甲基化与NSCLC相关性的研究。以比值比（odds ratio, OR）和95%置信区间（confidence interval, CI）为效应指标，分析RASSF1A基因启动子甲基化与NSCLC的关系。结果 共有23篇文献纳入本研究，RASSF1A基因启动子甲基化率在NSCLC患者肺部组织和对照组中分别为41.50%（95%CI: 34%-49%）和5.58%（95%CI: 2%-9%），meta分析显示肿瘤组织中的甲基化率高于对照组（OR=8.72, 95%CI:4.88-15.58, P<0.05）；亚组分析显示:肿瘤组织中的甲基化频率高于血浆（OR=10.99, 95%CI:2.48-48.68）和正常对照组织（OR=8.74, 95%CI: 4.39-17.41）。结论 NSCLC患者肺癌组织中RASSF1A基因启动子甲基化率高于对照组，组织中RASSF1A基因启动子甲基化率对肺癌的发生更具影响，RASSSF1A甲基化可能与肺癌的发生存在相关并可作为肺癌诊断的潜在标志物。.
背景与目的 肿瘤发生、发展过程中，抑癌基因启动子区域CpG岛异常甲基化起着重要的作用。已有研究显示RAS相关区域家族1A（Ras association domain family 1A, RASSF1A）基因，作为一个抑癌基因其启动子区域甲基化与非小细胞肺癌（non-small cell lung cancer, NSCLC）的发生发展密切相关。在NSCLC患者癌组织中RASSF1A基因启动子往往表现为异常高甲基化。本研究采用meta分析的方法探讨RASSF1A基因启动子甲基化与NSCLC发生之间的关系。方法 通过检索Medline、EMBASE、CNKI和万方数据库，按照已拟定的纳入与剔除标准筛选收集公开发表的关于RASSF1A基因启动子甲基化与NSCLC相关性的研究。以比值比（odds ratio, OR）和95%置信区间（confidence interval, CI）为效应指标，分析RASSF1A基因启动子甲基化与NSCLC的关系。结果 共有23篇文献纳入本研究，RASSF1A基因启动子甲基化率在NSCLC患者肺部组织和对照组中分别为41.50%（95%CI: 34%-49%）和5.58%（95%CI: 2%-9%），meta分析显示肿瘤组织中的甲基化率高于对照组（OR=8.72, 95%CI:4.88-15.58, P<0.05）；亚组分析显示:肿瘤组织中的甲基化频率高于血浆（OR=10.99, 95%CI:2.48-48.68）和正常对照组织（OR=8.74, 95%CI: 4.39-17.41）。结论 NSCLC患者肺癌组织中RASSF1A基因启动子甲基化率高于对照组，组织中RASSF1A基因启动子甲基化率对肺癌的发生更具影响，RASSSF1A甲基化可能与肺癌的发生存在相关并可作为肺癌诊断的潜在标志物。.