Analysis of DNAdamage checkpoint regulator gene and cancer control mechanism in oral cancer

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Damage and abnormality of DNA genome is the starting point of the process of malignant transformation of a normal cell. Once DNA damage occurs, eukaryotic cells can activate cell cycle checkpoints, apoptosis or senescence. Some kinases are related to cell cycle checkpoint, apoptosis and senescence pathways, and stimulate and activate other kinases. p53, a transcriptional factor mutated in over 50% of human cancers, is phosphorylated at Ser15 and Ser37 by ATM/ATR and DNA-PK. This phosphorylation promotes the accumulation and functional activation of p53 in response to DNA damage. Active Chk1 and Chk2 can phosphorylate p53 at several serine : sites, enhancing its tetramerization, stability and activity. In 60% of oral cancer, p53 is mutated. It seems that some kinds of oral cancer have different signal transmission pathways which are regarded as conventional DNA damage signal transmission pathways. We used several kinds of oral squamous carcinoma cell lines to check the expression of p53 first. After treatment with genotoxic stress to culture cells, we examined the expression of each protein in DNA damage checkpoint by Western blot analysis, and checked the localization in oral mucosal tissues by immunohistochemistry.