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Lysine methylation represses p53 activity in teratocarcinoma cancer cells

Jiajun Zhu1, Zhixun Dou2, Morgan A Sammons2

  • 1Epigenetics Program, Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104; Biomedical Graduate Studies, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104;

Proceedings of the National Academy of Sciences of the United States of America
|August 19, 2016
PubMed

Insights

Wild-type TP53 (tumor protein 53) activity is repressed by lysine methylation in testicular teratocarcinoma cells. Reducing methyltransferases reactivates p53, promoting cell differentiation and suggesting new therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • TP53 mutations are common in cancers, but wild-type TP53 function is also repressed in some tumors.
  • Testicular teratocarcinoma cells often retain wild-type TP53, yet p53 activity is suppressed despite high expression.

Purpose of the Study:

  • To investigate the mechanism of wild-type p53 repression in testicular teratocarcinoma.
  • To explore the role of post-translational modifications in p53 activity within these cancer cells.

Main Methods:

  • Analysis of p53 lysine methylation in the NTera2 teratocarcinoma cell line.
  • Manipulation of methyltransferase levels and expression of wild-type and mutant p53.
  • Assessment of p53 downstream target gene expression and cellular differentiation.

Main Results:

  • Endogenous wild-type p53 in NTera2 cells undergoes lysine methylation, repressing its transcriptional activity.
  • Depletion of methyltransferases reactivates p53 and induces NTera2 cell differentiation.
  • Methylation-deficient p53 mutants enhance p53 target gene expression and accelerate differentiation compared to wild-type p53.

Conclusions:

  • Lysine methylation of wild-type p53 is a key mechanism for repressing its tumor-suppressive function in testicular teratocarcinoma.
  • Targeting p53 methylation presents a potential therapeutic strategy for testicular cancers.
Keywords:
cancermethylationp53pluripotencyteratocarcinoma

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