细胞色素p450 2A13（CYP2A13）能代谢活化前致癌物产生致癌作用，其在非小细胞肺癌中的异常高表达与非小细胞肺癌发生密切相关。但CYP2A13这种异常高表达的调控机制目前尚不明确。本课题组发现，DNA甲基化抑制剂或组蛋白去乙酰化酶抑制剂单用对人肺上皮细胞BEAS-2B和鳞癌细胞H2170中CYP2A13的表达有上调作用，但幅度不大；而两者合用则能大幅上调CYP2A13的表达（分别为11倍和8倍）。鉴于表观遗传修饰在基因转录调控中的重要作用，我们推测：CYP2A13在非小细胞肺癌组织中的高表达受表观遗传修饰调控，并且DNA甲基化和组蛋白乙酰化的相互作用是其调控机制的关键。因此，本项目将研究DNA甲基化和组蛋白乙酰化及其相互作用对非小细胞肺癌中CYP2A13表达的影响和机理，从表观遗传的角度来阐明非小细胞肺癌中CYP2A13高表达的调控机制，以期为非小细胞肺癌的早期诊断提供新的思路。

CYP2A13 could activate procarcinogens in situ, and is highly expressed in non-small cell lung cancer tissue compared with normal lung tissue. There is a significant association of the abnormal high expression of CYP2A13 with lung carcinogenesis. But up to now, the mechanism of such abnormal expression remains unknown. It is reported that the abnormal expressions of multiple genes in tumor tissues are regulated by epigenetic modification. Our previous investigations showed that combined treatment with AzaC (a DNA demethylation agent) and TSA (an inhibitor of HDAC) could up-regulate CYP2A13 expression in BEAS-2B and H2170 cells, 11-fold and 8-fold respectively, which is far more than treatment with either AzaC or TSA alone. Therefore, we speculate that the high expression of CYP2A13 in non-small cell lung cancer is epigenetically regulated and the interaction patterns of DNA methylation and histone acetylation may play a key role. In this study, the effects of DNA methylation, histone acetylation and their interaction on CYP2A13 expression will be a investigated, to clarified the regulation mechanism of the abnormal high expression of CYP2A13 in non-small cell lung cancer in a epigenetic way. Our works may provide a new approach for early detection for non-small cell lung cancer.