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p53 controls expression of the DNA deaminase APOBEC3B to limit its potential mutagenic activity in cancer cells

Manikandan Periyasamy1, Anup K Singh1, Carolina Gemma1

  • 1Department of Surgery & Cancer, Imperial College London, Hammersmith Hospital Campus, London W12 0NN, UK.

Nucleic Acids Research
|October 5, 2017
PubMed

Insights

The tumor suppressor p53 normally suppresses APOBEC3B (A3B) gene expression. Loss of p53 function in cancer leads to increased A3B activity, promoting cancer mutagenesis.

Area of Science:

  • Molecular Biology
  • Cancer Genetics
  • Genomics

Background:

  • Apolipoprotein B mRNA editing enzyme catalytic polypeptide-like (APOBEC) genes, particularly APOBEC3B (A3B), are implicated in cancer mutagenesis.
  • Understanding the regulation of A3B expression is crucial for developing targeted cancer therapies.

Purpose of the Study:

  • To investigate the regulatory mechanisms controlling A3B gene expression in cancer.
  • To elucidate the relationship between p53 status and A3B overexpression.

Main Methods:

  • Analysis of A3B expression in relation to p53 status across various cancer types.
  • Investigating the role of p53 in repressing A3B expression via p21 (CDKN1A) and the DREAM complex.
  • Assessing the impact of p53 loss (mutation or HPV inhibition) on A3B promoter activity.

Main Results:

  • A3B expression is inversely correlated with p53 status in diverse cancers.
  • p53 directly represses A3B expression by inducing p21 (CDKN1A).
  • p53 facilitates the recruitment of the repressive DREAM complex to the A3B promoter, which is impaired upon p53 loss.

Conclusions:

  • Loss of p53 function, common in cancer, leads to derepression of A3B, increasing its cytosine deaminase activity and promoting cancer mutagenesis.
  • Targeting A3B or understanding its regulation in the context of p53 status may offer therapeutic strategies.

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