Respiratory Carcinogenesis

D Pastuszak-Lewandoska, K H Czarnecka, M Migdalska-Sęk, E Nawrot, D Domańska, J Kiszałkiewicz, J Kordiak, A Antczak, P Górski, E Brzeziańska-Lasota, D. Pastuszak-Lewandoska, K. H. Czarnecka, M. Migdalska-Sęk, E. Nawrot, D. Domańska, J. Kiszałkiewicz, J. Kordiak, A. Antczak, P. Górski, E. Brzeziańska-Lasota, Pastuszak-Lewandoska, D., Czarnecka, K. H., Migdalska-Sęk, M., Nawrot, E., Domańska, D., Kiszałkiewicz, J., Kordiak, J., Antczak, A., Górski, P., Brzeziańska-Lasota, E.

Lung cancer is the leading cause of cancer-related death in the world. Early detection, based on molecular markers, could decrease mortality from this disease. Tumor development is often associated with inactivation or loss of tumor suppressor genes (TSGs). The aim of the present study was to analyze the expression level of FAM107A gene, a TSG located in 3p21.1, in lung cancer tumors and in tumor adjacent normal lung samples. Promoter methylation status of FAM107A was evaluated as the potential mechanism of its epigenetic silencing. The relationship between gene mRNA expression and tumor staging, metastasis status, and non-small cell lung cancer (NSCLC) histopathological subtypes in 60 patients was analyzed. Total RNA was isolated from tissue samples and gene expression was assessed in qPCR assay. Gene promoter methylation status was evaluated in MSP reactions, using bisulfite converted DNA and two pairs of primers: methylated and unmethylated. We found that the expression of the gene was dramatically decreased in all NSCLC samples and was significantly lower than in tumor adjacent normal lung tissue. Promoter methylation of FAM107A gene was confirmed only in the minority of NSCLCs. The results highlight the importance of FAM107A in lung carcinogenesis, although indicate other than promoter hypermethylation mechanism of the gene decreased expression.