Accumulation of p16CDKN2A in response to ultraviolet irradiation correlates with late S-G(2)-phase cell cycle delay.

p16 is the product of the CDKN2A locus, which is mutated or deleted in many human tumors. In response to nonlethal UVC irradiation, HeLa cells accumulate elevated levels of p16. The accumulation of p16 is delayed 8-12 h following irradiation and correlates with S-phase and G2 delays, decreasing as the cells recover and recommence normal cell growth. The maximum levels of p16 correlated with G2 delay. The UVC-induced cell cycle delay was absent in cell lines derived from HeLa that did not express p16 and in a melanoma line deleted for p16.