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Significance Cancer progression typically involves inactivation of the p53 tumor suppressor. In testicular teratocarcinoma, there exist unusually high protein levels of wild-type p53, but strikingly, without normal activation of genes up-regulated by p53, such as cell cycle arrest and DNA repair pathways. This suggests that posttranslational mechanisms, such as protein modification, may repress activity of the high levels of wild-type p53. Our findings demonstrate an important role in teratocarcinoma of previously characterized repressive p53 methylation, which down-regulates normal p53 activation functions. The results suggest the potential for novel approaches to reactivate wild-type p53 in teratocarcinoma via therapeutic inhibition of the methyltransferase enzymes that modify p53, which could be similarly appropriate for treatment of other cancers expressing high levels of wild-type p53.

Lysine methylation represses p53 activity in teratocarcinoma cancer cells