Determination of rassfa1 and sparcl1 gene methylation levels in lung adenocarcinoma

Cell functions; including cell cycle control, cellular differentiation, signaling, and apoptosis, can be controlled with transcriptional silencing via DNA methylation process. In normal cells, the promotor CpG islands in specific genes are usually in the unmethylated state, although the genome is globally methylated. In cancer, the promotor methylation in the tumor suppressor genes, is a prematurely emerging event besides global hypomethylation. Studies in the literature suggest an association between the status of methylation in the tumor suppressor genes and the prognosis of lung adenocarcinoma; proposing that these genes can be used as biomarkers to predict the prognosis. The aim of this study is to determine the methylation status of RASSF1A and SPARCL1 genes in lung adenocarcinoma, the most common type of non-small cell lung carcinomas. 40 tumor tissues and 40 normal tissues from 40 patients with lung adenocarcinoma, were included in the study. Following DNA isolation from the paraffin embedded tissue samples, bisulfite application was performed and then, the methylation in the RASSF1A and SPARCL1 genes were analyzed with the real-time PCR method. In our study, the frequency of methylation in RASSF1A and SPARCL1 were found to be 42,5% and 32,5%, respectively. The status of methylation was significantly higher in the lung adenocarcinoma tissues compared to the control tissues (p=0.000), however; there were no associations between the clinicopathological parameters and the status of methylation. Our study is the first one that evaluates the status of methylation in the RASSF1A and SPARCL1 genes together, at the same time in the adenocarcinomatous tumor tissues of Turkish patients. It is found that the results of the current study are parallel with the results of other similarly designed studies.