Clarification of reguratory mechanism of cell proliferation by HTLV-1.

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Human T-cell leukemia virus type 1 (HTLV-1) is a causative agent for the development of adult T-cell leukemia (ATL). Tax encoded by HTLV-1 plays important role in immortalization of primary human lymphocytes. This capacity of Tax is conducted by modulation of cellular genes regulated by CREB, NFkB. We previously reported that p53, a suppresser oncogene, is also regulated its transacting function by Tax. Purpose in this work is to clarify molecular mechanism of Tax to suppress p53 trans-acting function. We observed that p53 accumulates in cells expressing Tax. Tax mutant which lacks to bind CBP/p300 failed to suppress p53 trans-acting function, suggested that Tax regulates p53 function through interaction with CBP/p300. From binding analysis of CBP/p300 with p53 or Tax, we concluded that suppressive effect of Tax for p53 function is occurred by competitive association with CBP/p300. Suppressive effect of Tax to p53 family gene products other than p53 was also occurred by the similar mechanism seen in p53.