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PARP-1 is involved in autophagy induced by DNA damage

José Antonio Muñoz-Gámez1, José Manuel Rodríguez-Vargas, Rosa Quiles-Pérez

  • 1Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (Ciberehd) and Laboratory of Medical Research, Academical Hospital San Cecilio, Granada, Spain.

Autophagy
|November 13, 2008
PubMed

Insights

Poly(ADP-ribose) polymerase-1 (PARP-1) activation is crucial for initiating autophagy, a protective cellular process, in response to DNA damage from chemotherapy. PARP-1 deficiency prevents this protective autophagy, leading to increased cell death.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Oncology

Background:

  • Autophagy is a cellular degradation process often activated in cancer cells during chemotherapy or radiation treatment.
  • Poly(ADP-ribose) polymerase-1 (PARP-1) inhibition enhances chemotherapy-induced cell death, but its role in DNA damage-induced autophagy remains unclear.

Purpose of the Study:

  • To investigate the role of PARP-1 in the cellular decision to undergo autophagy following DNA damage.
  • To determine if PARP-1 activation is necessary for doxorubicin-induced autophagy.

Main Methods:

  • Treatment of PARP-1 wild-type and deficient cells with doxorubicin.
  • Analysis of autophagic vesicles via electron microscopy and GFP-LC3 transfection.
  • Gene expression analysis of autophagy-related genes (bnip-3, cathepsin b and l, beclin-1).
  • Assessment of ATP/NAD+ levels and mTOR activation.

Main Results:

  • Doxorubicin treatment induced autophagic vesicles and increased autophagy gene expression in wild-type cells, but not in PARP-1 deficient cells or cells treated with a PARP inhibitor.
  • Lack of autophagy in PARP-1 deficient/inhibited cells was linked to prevention of ATP/NAD+ depletion and mTOR activation.
  • Inhibition of doxorubicin-induced autophagy led to increased cell death, indicating a protective role for autophagy.

Conclusions:

  • PARP-1 activation is involved in the cellular decision to initiate autophagy in response to DNA damage.
  • Doxorubicin-induced autophagy appears to be a cytoprotective mechanism against DNA damage.
  • Targeting PARP-1 may influence the efficacy of chemotherapy by modulating autophagy.

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