engleski

Reduced promoter methyilation of MyD88 and ASC/TMS1 genes in tumor tissue of patients with lung and larynx carcinoma

Aberrant DNA methylation of promoter region CpG islands is associated with gene silencing and serves as an alternative to mutation-induced inactivation of tumor suppressor genes in human cancers. Chronic inflammation and infection have been recognized among major risk factors for the most common types of cancer. Several lines of evidences are linking cancer, inflammation and infection. For example, transcription factor nuclear factor-κB (NF-κB), major inducer of inflammation is activated by many cancer risk factors (cigarettes smoke) and is constitutively active in most cancer. Many epidemiological studies have shown that inflammatory/infection conditions precede most cancers. Activation and controlling mechanisms of inflammation and infection are regulated by NF-κB and almost exclusively relied on receptors of innate immunity, known as Pattern Recognition Receptors (PRR). Thus, suppression of these proinflammatory pathways may provide opportunities for both prevention and treatment of cancer. The aim of presented study was to evaluate methylation status of ASC/TMS1 and MyD88 genes, key adaptor molecules in innate immunity signaling. We were using pyrosequencing approach, method that is still golden standard in methylation analysis, to define methylation status of promoter regions of genes of interest. Here we found that both MyD88 and ASC/TMS1 exhibit reduced methylation status of promoter regions in tested tumor tissues, comparing to healthy tissue. Also, we found different methylation pattern of specific tested CpG islands characteristic for lung and larynx cancer.

methylation, inflammation, cancer, MyD88, ASC/TMS1

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