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A comparison of p53 and p16 expression in human tumor cells treated with hyperthermia or ionizing radiation
Author(s) -
Valenzuela María Teresa,
Núñez María Isabel,
Villalobos Mercedes,
Siles Eva,
McMillan Trevor J.,
Pedraza Vicente,
Ruiz de Almodóvar J. Mariano
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19970717)72:2<307::aid-ijc18>3.0.co;2-c
Subject(s) - ionizing radiation , hyperthermia , intracellular , cell culture , cancer research , cell cycle checkpoint , cell cycle , cell , biology , microbiology and biotechnology , irradiation , chemistry , biochemistry , genetics , physics , paleontology , nuclear physics
To assess the potential relationship between p53 and p16 proteins in the cellular response to stress, we have examined the levels of these proteins in a series of human tumor cell lines after treatment with either ionizing radiation or hyperthermia. We found that cells with abnormal radiation‐induced G 1 arrest (non‐functional p53) had significantly higher constitutive levels of p16 than cells showing a normal G 1 arrest (functional p53). Time‐course experiments were done to test the effect of γ‐irradiation on intracellular levels of p16. The pattern of changes in p16 response was similar in all cell lines studied, and p16 expression was not related to cellular sensitivity to radiation or to the level of p53 induction after treatment. We also provide evidence that short‐term exposure to high temperature causes p53 accumulation. Hyperthermia‐induced p53 accumulation was greatest in those cells exhibiting the highest radiation‐induced p53 accumulation, suggesting a possible relationship between p53 induction after these 2 different stresses. p16 synthesis was also induced in different cell lines after heat treatment, and this response was independent of p53 functionality. When we compared the level of p16 expression with the extent of G 0 /G 1 arrest induced by heat, a linear correlation was found, raising the possibility that p16 may be involved in the control of cell cycle progression in response to heat treatment. Int. J. Cancer 72:307–312, 1997. © 1997 Wiley‐Liss, Inc.