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Accumulation of p16^CDKN2A in Response to Ultraviolet Irradiation Correlates with a Late S-G₂-Phase Cell Cycle Delay¹

Queensland Cancer Fund Research Unit, Queensland Institute of Medical Research, The Bancroft Center, P. O. Royal Brisbane Hospital, Brisbane 4029, Queensland, Australia

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.

¹ This work was supported by grants from the National Health and Medical Research Council and the Queensland Cancer Fund. B. G. is a Fuiczek Fellowship holder.

² To whom requests for reprints should be addressed. Fax: (07) 3362 0107; E-mail brianG@qimr.edu.au.

Received 3/ 4/96. Accepted 4/17/96.

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