Abstract
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.
Highlights
Lung cancer is the leading cause of cancer-related death in males and females worldwide (Ginsberg, 1997; Marby, Nelkin, & Baylin, 1998)
This study showed that expression and methylation level of KMT2D and IGF2 genes did not change in non- small cell lung cancer (NSCLC) tumor samples compared to normal samples
There was no significant difference between the expression of this gene in tumor samples compared to normal samples (P = 0.46). (Figure 1.A shows the result of the KMT2D gene expression)
Summary
Lung cancer is the leading cause of cancer-related death in males and females worldwide (Ginsberg, 1997; Marby, Nelkin, & Baylin, 1998). Previous studies have demonstrated that lung cancer development involves environmental, genetic and epigenetic factors Epidemiological studies indicate that cigarette smoking, as well as exposure to asbestos and radon, have a strong causal association with lung cancer (Alberg, Ford, & Samet, 2007). Somatic genetic aberrations, such as mutations and copy number alterations, play a well-known role in oncogenesis, epigenetic alterations are more frequent than somatic mutations in lung cancer (Brzeziańska, Dutkowska, & Antczak, 2013). The expression and methylation of KMT2D and IGF2 genes were investigated in the lung cancer tissue compared to the adjacent normal tissue
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