Zarandi Ashkan, Irani Shiva, Savabkar Sanaz, Chaleshi Vahid, Ghavideldarestani Maryam, Mirfakhraie Reza, Khodadoostan Mahsa, Nazemalhosseini-Mojarad Ehsan, Asadzadeh Aghdaei Hamid
Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Basic and Molecular Epidemiology of Gastrointestinal Disorders Research Center, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Gastroenterol Hepatol Bed Bench. 2017 Winter;10(Suppl1):S117-S121.
The aim of this study was to evaluate the methylation status of the promoter region of MLH1 gene in colorectal cancer (CRC) and its precursor lesions as well as elucidate its association with various clinicopathological characteristics among Iranian population.
Epigenetic silencing of mismatch repair genes, such as , by methylation of CpG islands of their promoter region has been proved to be an important mechanism in colorectal carcinogenesis.
Fifty colorectal cancer and polyp tissue samples including 13 Primary colorectal tumor and 37 Adenoma polyp samples were enrolled in this study. Methylation-specific polymerase chain reaction (MSP) was performed to find the frequency of MLH1 Promoter Methylation.
Promoter methylation of gene was detected in 5 out of 13 tumor tissues and 4 out of 37 adenoma polyp. The frequency of methylation in tumor samples was significantly higher compared to that in polyp tissues (P= 0.026). No significant association was observed between promoter methylation and clinicopathological characteristics of the patients.
The frequency of promoter methylation in CRC and colon polyp was 18%. Our findings indicated that methylation of promoter region alone cannot be considered as a biomarker for early detection of CRC.
本研究旨在评估伊朗人群中结直肠癌(CRC)及其癌前病变中MLH1基因启动子区域的甲基化状态,并阐明其与各种临床病理特征的关系。
错配修复基因的表观遗传沉默,如通过其启动子区域的CpG岛甲基化,已被证明是结直肠癌发生的重要机制。
本研究纳入了50份结直肠癌和息肉组织样本,包括13份原发性结直肠癌肿瘤样本和37份腺瘤性息肉样本。采用甲基化特异性聚合酶链反应(MSP)检测MLH1启动子甲基化的频率。
在13份肿瘤组织中有5份检测到基因启动子甲基化,在37份腺瘤性息肉中有4份检测到。肿瘤样本中的甲基化频率明显高于息肉组织(P = 0.°26)。未观察到启动子甲基化与患者临床病理特征之间存在显著关联。
CRC和结肠息肉中启动子甲基化的频率为18%。我们的研究结果表明,仅启动子区域的甲基化不能被视为CRC早期检测的生物标志物。