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A function for cyclin D1 in DNA repair uncovered by protein interactome analyses in human cancers

Siwanon Jirawatnotai1, Yiduo Hu, Wojciech Michowski

  • 1Department of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02215, USA.

Nature
|June 10, 2011
PubMed

Insights

Cyclin D1, a cell cycle protein, unexpectedly aids DNA repair by binding RAD51 at damage sites. Inhibiting cyclin D1 may treat retinoblastoma-negative cancers, expanding its therapeutic potential.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • DNA Repair Mechanisms

Background:

  • Cyclin D1 is a key cell cycle regulator frequently overexpressed in human cancers.
  • Its precise role in cancer beyond cell cycle progression remains incompletely understood.

Purpose of the Study:

  • To identify novel molecular functions of cyclin D1 in human cancer.
  • To investigate the interaction between cyclin D1 and DNA repair pathways.

Main Methods:

  • Proteomic screening to identify cyclin D1 interacting proteins in human tumors.
  • Co-immunoprecipitation and immunofluorescence to study protein interactions and localization.
  • Assessment of DNA repair capacity and cellular sensitivity to radiation upon cyclin D1 depletion.

Main Results:

  • Proteomic analysis revealed that cyclin D1 interacts with DNA repair proteins, notably RAD51.
  • Cyclin D1 directly binds RAD51, and this interaction is radiation-induced and BRCA2-dependent.
  • Depletion of cyclin D1 impairs RAD51 recruitment to DNA damage sites, hinders homologous recombination repair, and increases radiosensitivity, even in retinoblastoma-negative cancer cells.

Conclusions:

  • Cyclin D1 possesses a previously unrecognized function in homologous recombination-mediated DNA repair.
  • Targeting cyclin D1 may offer therapeutic benefits for retinoblastoma-negative cancers, a group not typically considered responsive to cyclin D1 inhibition.

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