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Acetylation of p62 regulates base excision repair through interaction with APE1

Meiting Li1, Jiannan Xiong2, Liqian Yang2

  • 1Beijing Key Laboratory of Protein Posttranslational Modifications and Cell Function, Department of Biochemistry and Biophysics, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China; Department of Medical Genetics, Center for Medical Genetics, Peking University Health Science Center, Beijing 100191, China.

Cell Reports
|July 20, 2022
PubMed

Insights

p62 protein regulates base excision repair (BER) in cancer cells. Loss of p62 increases sensitivity to DNA damaging agents, highlighting its role in cancer therapy.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • DNA Repair

Background:

  • p62 is a known autophagy adaptor involved in stress responses.
  • Its role in DNA repair pathways has not been previously established.

Purpose of the Study:

  • To investigate the function of p62 in base excision repair (BER).
  • To determine the therapeutic potential of targeting p62 in cancer.

Main Methods:

  • Assessed BER capacity in p62-deficient cancer cells.
  • Examined p62 localization and modification (acetylation/deacetylation) upon DNA damage.
  • Investigated the interaction of p62 with APE1 and its effect on endonuclease activity.

Main Results:

  • Loss of p62 impairs BER and sensitizes cancer cells to alkylating and oxidizing agents.
  • p62 accumulates in the nucleus, is acetylated by hMOF, and deacetylated by SIRT7 in response to damage.
  • Acetylated p62 recruits to chromatin and enhances APE1 endonuclease activity, promoting BER and cell survival.

Conclusions:

  • p62 acts as a novel regulator of the base excision repair pathway.
  • Targeting p62 represents a potential therapeutic strategy for cancer treatment.
Keywords:
APE1CP: Molecular biologySIRT7acetylationbase excision repairhMOFp62

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