Abstract: BACKGROUND ＆ AIM: To study the aberrant DNA methylation of genomic DNA in lung cancer tissues as a possible epigenetic mechanism in the development of lung cancer. MATERIAL AND METHODS: Genomic DNA isolated from lung cancer and its adjacent tissue was restriction digested with Mse1 (methylation non-sensitive) alone or with Mse1 and BstU1 (methylation sensitive). The resulting DNA was analyzed for aberrant methylation using a PCR-based technique- Methylation-sensitive Restriction Fingerprinting (MSRF). Several DNA fragments differentially methylated in the transformed cells compared with the non-transformed cells were identified by MSRF. These fragments were subcloned, sequenced and compared with GenBank. At the same time, the DNA methylation was analyzed according to age, sex and smoking status. RESULTS: As compared with the control tissues, 84.5％ (49/58) of lung cancer tissues were found to have aberrant DNA methylation, but the methylation rate did not differ significantly among the squamous carcinoma (82.1％), and adenocarcinoma (88.5％) and other cancer types (75.0％)(χ2=0.073, P>0.05). Among the fragments methylated, 83％ was hypermethylated and 17％ was hypomethylated. We have identified the fragments encoding for human cyclin C (CCNC) and Wilms tumor (WT-1). When smoking, age and sex were considered as factors, no significant differences were observed. CONCLUSION: The aberrant DNA methylation, especially hypermethylation, seemed to play an important role in the development of lung cancer. It appeared to be a possible epigenetic mechanism for lung cancer.

Key words: lung cancer, genomic DNA, methylation