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p16 and p53 after different treatments in human-tumour cells.

Research output: Contribution to Journal/MagazineJournal article

  • M. T. Valenzuela
  • M. I. Núñez
  • E. Siles
  • M. Villalobos
  • V. Pedraza
  • A. T. Gordon
  • T. J. McMillan
  • J. M. R. de Almodóvar
<mark>Journal publication date</mark>1995
<mark>Journal</mark>European Journal of Cancer
Issue numberSupple
Pages (from-to)S175-S175
Publication StatusPublished
<mark>Original language</mark>English


It has been suggested that the product of p53 gene inhibits cellular growth by stimulating the production of p16 protein. We have examined by ELISA the protein levels of p16 (ranged 0.80-3.44 O.D. unit per 106 cells) and p53 (ranged 2.20-4.65 O.D. unit per 106 cells) in human tumour cell lines. We have not found a quantitative relationship between these protein levels: neither in standard growth conditions nor after 6 Gy of radiation. The p53 product function has been surveyed by flow cytometry studying cell cycle arrest after irradiation of the cells at 6 Gy. Taking into account that concept we have divided our cell lines in two groups (A) cells with functional p53 protein and (B) cells with functional inactivation of the p53 gene product. Higher constitutive levels of p16 product were found in group A cells. Intracellular p16 levels change after 6 Gy but not a defined time course profile has been found. We have identified that p16 levels change markedly with growth conditions, ie, age of culture, growth rate modified by use of differents serum levels or after hormonal synchronization of human breast cancer cell lines. The implications of this for the radiation response and cellular proliferation of human tumour cell lines remains to be determined.