Eskandari-Nasab Ebrahim, Hashemi Mohammad, Rafighdoost Firoozeh
Genetics of Non-Communicable Disease Research Center, Zahedan University of Medical Sciences, Zahedan 9816743463, Iran; Department of Clinical Biochemistry, School of Medicine, Zahedan University of Medical Sciences, Zahedan 9816743463, Iran.
Department of Clinical Biochemistry, School of Medicine, Zahedan University of Medical Sciences, Zahedan 9816743463, Iran.
J Cancer Epidemiol. 2016;2016:7680523. doi: 10.1155/2016/7680523. Epub 2016 Mar 29.
Background. Response gene to complement 32 (RGC32), induced by activation of complements, has been characterized as a cell cycle regulator; however, its role in carcinogenesis is still controversial. In the present study we compared RGC32 promoter methylation patterns and mRNA expression in breast cancerous tissues and adjacent normal tissues. Materials and Methods. Sixty-three breast cancer tissues and 63 adjacent nonneoplastic tissues were included in our study. Design. Nested methylation-specific polymerase chain reaction (Nested-MSP) and quantitative PCR (qPCR) were used to determine RGC32 promoter methylation status and its mRNA expression levels, respectively. Results. RGC32 methylation pattern was not different between breast cancerous tissue and adjacent nonneoplastic tissue (OR = 2.30, 95% CI = 0.95-5.54). However, qPCR analysis displayed higher levels of RGC32 mRNA in breast cancerous tissues than in noncancerous tissues (1.073 versus 0.959; P = 0.001), irrespective of the promoter methylation status. The expression levels and promoter methylation of RGC32 were not correlated with any of patients' clinical characteristics (P > 0.05). Conclusion. Our findings confirmed upregulation of RGC32 in breast cancerous tumors, but it was not associated with promoter methylation patterns.
背景。补体反应基因32（RGC32）由补体激活诱导产生，已被表征为一种细胞周期调节因子；然而，其在致癌作用中的角色仍存在争议。在本研究中，我们比较了乳腺癌组织和癌旁正常组织中RGC32启动子甲基化模式及mRNA表达。
材料与方法。我们的研究纳入了63例乳腺癌组织和63例癌旁非肿瘤组织。
设计。分别采用巢式甲基化特异性聚合酶链反应（Nested-MSP）和定量PCR（qPCR）来确定RGC32启动子甲基化状态及其mRNA表达水平。
结果。乳腺癌组织与癌旁非肿瘤组织之间的RGC32甲基化模式无差异（OR = 2.30，95%可信区间 = 0.95 - 5.54）。然而，qPCR分析显示，无论启动子甲基化状态如何，乳腺癌组织中RGC32 mRNA水平均高于非癌组织（1.073对0.959；P = 0.001）。RGC32的表达水平及启动子甲基化与患者的任何临床特征均无相关性（P > 0.05）。
结论。我们的研究结果证实乳腺癌肿瘤中RGC32上调，但这与启动子甲基化模式无关。
