Retinoblastoma family proteins: New players in DNA repair by non-homologous end-joining.
Loss of retinoblastoma protein (RB1) function is a major driver in cancer development. We have recently reported that, in addition to its well-documented functions in cell cycle and fate control, RB1 and its paralogs have a novel role in regulating DNA repair by non-homologous end joining (NHEJ). Here we summarize our findings and present mechanistic hypotheses on how RB1 may support the DNA repair process and the therapeutic implications for patients who harbor RB1-negative cancers.
The Institute of Cancer Research, Division of Cancer Biology, Chester Beatty Laboratories , London, UK.
Paul H
PH
Huang
The Institute of Cancer Research, Division of Cancer Biology, Chester Beatty Laboratories, London, UK; Cancer Cell Signalling, UCL Cancer Institute, University College London, London, UK.
Rebecca
R
Cook
The Institute of Cancer Research, Division of Cancer Biology, Chester Beatty Laboratories , London, UK.
Georgia
G
Zoumpoulidou
The Institute of Cancer Research, Division of Cancer Biology, Chester Beatty Laboratories , London, UK.
Maciej T
MT
Luczynski
The Institute of Cancer Research, Division of Cancer Biology, Chester Beatty Laboratories, London, UK; Cancer Cell Signalling, UCL Cancer Institute, University College London, London, UK.
Sibylle
S
Mittnacht
DNA repair; non-homologous end-joining; retinoblastoma protein; tumor suppressor