Background Colorectal cancer is common among obese individuals. The purpose of the current study was to determine changes in DNA methylation status and mRNA expression of thyroid hormone receptor beta (THRB), as a tumor suppressor, and thyroid hormone inactivating enzyme, type 3 deiodinase (DIO3) genes, in human epithelial colon tissues of healthy obese individuals. Methods Colon biopsies were analyzed by methylation sensitive-high resolution melting (MS-HRM) to investigate promoter methylation of DIO3 and THRB, and by quantitative real-time polymerase chain reaction to assay expression of DIO3 and THRB mRNA on eighteen obese and twenty-one normal-weight healthy men. Results There was no significant difference in mean methylation levels at the THRB promoter region between the two groups. Nevertheless, obesity decreased THRB expression levels, significantly (P < 0.05; fold change: 0.19). Furthermore, obesity attenuated DNA methylation (P < 0.001) and enhanced mRNA expression of DIO3 (P < 0.05; fold change: 3). Conclusions Our findings suggest that obesity may alter expression of THRB and DIO3 genes through epigenetic mechanism. Alterations of THRB and DIO3 expressions may predispose colon epithelium of obese patients to neoplastic transformation.

Background: Aberrant promoter methylation of CpG islands is an important mechanism for regulation of gene expression. Recent data suggest that epigenetic abnormalities may occur very early in lung carcinogenesis. Systemic methylation changes may be a diagnostic marker for tumor development or prognosis. In this study, the expression and methylation of KMT2D and IGF2 genes were investigated in the lung cancer tissue compared to the adjacent normal tissue. Methods:The status of methylation of KMT2D and IGF2 genes were investigated in 30 patients with NSCLC after genomic DNA extraction using bisulfite treatment and MS-HRM method and the expression of these genes were checked by Real-Time PCR method in same samples.Results: For KMT2D gene, the expression and methylation level increased in 46.6% and 6.67% (respectively) for tumor samples comparison with normal samples (P>0.05). Also, for IGF2 gene 50% tumor samples overexpressed and 50% tumor samples showed that reduced expression comparison with the normal samples (P>0.05). In addition, 96.66% of tumor tissues did not show any change in methylation level for IGF2 gene promoter (P>0.05). Conclusion:This study showed that expression and methylation level of KMT2D and IGF2 genes did not change in NSCLC tumor samples compared to normal samples. However, this study was designed as a pilot study, and further investigations are required to confirm our findings.

Background: Lung cancer is the leading cause of cancer-related deaths worldwide and the 5-year survival rate is still very poor due to the lack of effective tools for early detection. Epigenetics and especially studies on DNA methylation have given important information towards a better achievement of lung cancer pathogenesis in the recent decades. The inactivation of tumor suppressor genes via promoter hypermethylation is an obvious mechanism and is straightly related to carcinogenesis. In this study, we compared the methylation status of KLF11 and PCDH9 genes in non-small cell lung cancer and adjacent normal tissues.Methods: Genomic DNA was extracted from 30 tumor tissues, bisulfite treated and were analyzed in terms of promoter methylation status of KLF11 and PCDH9 genes by high resolution melting method. Statistical analysis was carried out by chi-square test.Results: No significant difference in methylation level at the PCDH9 promoter region in NSCLC tumors compared with non-tumor tissues was observed (P = 0.3132, chi-square test). In contrast, the difference in methylation levels between normal and tumor tissue samples for the promoter of the KLF11 gene was quite significant (P = 0.0001).Conclusions: Promoter methylation of KLF11 gene is an important mechanism in the development of NSCLC, therefore, it could be used as one of the potential therapeutic goals for molecular targeted therapy and epigenetic treatment. The role of the PCDH9 gene in the development of lung cancer is complex and requires more research and a larger statistical population.