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Pyruvate kinase M2 interacts with DNA damage-binding protein 2 and reduces cell survival upon UV irradiation

Xiao Xie1, Mingsong Wang1, Ju Mei1

  • 1Department of Cardiothoracic Surgery, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200092, China.

Biochemical and Biophysical Research Communications
|September 28, 2015
PubMed

Insights

Pyruvate Kinase M2 (PKM2) interacts with DNA Damage-Binding Protein 2 (DDB2), impacting DNA repair and cell survival after UV exposure. This PKM2 regulation of DDB2 offers insights into UV-induced tumorigenesis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biochemistry

Background:

  • Pyruvate Kinase M2 (PKM2) is frequently overexpressed in solid tumors, contributing to metabolic reprogramming and tumor proliferation.
  • DNA Damage-Binding Protein 2 (DDB2) plays a critical role in the nucleotide excision repair pathway, essential for repairing UV-induced DNA damage.

Purpose of the Study:

  • To investigate the potential interaction between PKM2 and DDB2.
  • To elucidate the role of PKM2 in regulating DDB2 function and DNA repair.
  • To explore the implications of this interaction in UV-induced DNA damage and tumorigenesis.

Main Methods:

  • Co-immunoprecipitation assays to confirm PKM2-DDB2 binding.
  • Western blotting to assess DDB2 phosphorylation and DDB2-DDB1 complex formation.
  • Cell viability assays following UV irradiation in PKM2 knockdown and overexpression models.

Main Results:

  • PKM2 directly binds to DDB2, a process enhanced by UV irradiation and K433 acetylation of PKM2.
  • Overexpression of PKM2 promotes DDB2 phosphorylation and disrupts the DDB2-DDB1 interaction.
  • PKM2 knockdown enhances cell survival after UV exposure, while PKM2 overexpression reduces it; DDB2-DDB1 overexpression can reverse this effect.

Conclusions:

  • PKM2 regulates DDB2 function, affecting DNA repair capacity and cellular response to UV damage.
  • This novel PKM2-DDB2 interaction provides a potential molecular mechanism contributing to UV-induced tumorigenesis.
  • Targeting the PKM2-DDB2 pathway may offer new therapeutic strategies for UV-related cancers.
Keywords:
Cell survivalDDB2PKM2TumorigenesisUV

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