Min Liu1,2, Hongyan Wang2, Solah Lee2, Bailong Liu1,2, Lihua Dong1, Ya Wang2. 1. a Department of Radiation Oncology , the First Hospital, Jilin University , Changchun , China. 2. b Department of Radiation Oncology , School of Medicine and the Winship Cancer Institute, Emory University , Atlanta , Georgia , USA.
Abstract
PURPOSE: To clarify which DNA double-strand break repair pathway, non-homologous end-joining (NHEJ), homologous recombination repair (HRR) or both, plays a key role in potentially lethal damage repair (PLDR). METHODS AND MATERIALS: Combining published data and our new potentially lethal damage repair (PLDR) data, we explain whether similar to sublethal damage repair (SLDR), PLDR also mainly depends on NHEJ versus HRR. The PLDR data used the same cell lines: wild type, HRR or NHEJ-deficient fibroblast cells, as those SLDR data published by our laboratory previously. The PLDR condition that we used was as commonly described by many other groups: the cells were collected immediately or overnight post ionizing radiation for colony formation after cultured to a plateau phase with a low concentration of serum medium. RESULTS: Enough data from other groups and our lab showed that wild type or HRR-deficient cells had efficient PLDR, but NHEJ deficient cells did not. CONCLUSION: NHEJ contributes more to PLDR than HRR in mammalian cells, which is similar to SLDR. Since both SLDR and PLDR are relevant to clinical tumor status while undergoing radiotherapy, such clarification may benefit radiotherapy in the near future.
PURPOSE: To clarify which DNA double-strand break repair pathway, non-homologous end-joining (NHEJ), homologous recombination repair (HRR) or both, plays a key role in potentially lethal damage repair (PLDR). METHODS AND MATERIALS: Combining published data and our new potentially lethal damage repair (PLDR) data, we explain whether similar to sublethal damage repair (SLDR), PLDR also mainly depends on NHEJ versus HRR. The PLDR data used the same cell lines: wild type, HRR or NHEJ-deficient fibroblast cells, as those SLDR data published by our laboratory previously. The PLDR condition that we used was as commonly described by many other groups: the cells were collected immediately or overnight post ionizing radiation for colony formation after cultured to a plateau phase with a low concentration of serum medium. RESULTS: Enough data from other groups and our lab showed that wild type or HRR-deficient cells had efficient PLDR, but NHEJ deficient cells did not. CONCLUSION: NHEJ contributes more to PLDR than HRR in mammalian cells, which is similar to SLDR. Since both SLDR and PLDR are relevant to clinical tumor status while undergoing radiotherapy, such clarification may benefit radiotherapy in the near future.
Entities:
Keywords:
DNA double strand break (DSB); DNA repair; homologous recombination repair (HRR); ionizing radiation; non-homologous end-joining (NHEJ); sublethal damage repair (SLDR); potentially lethal damage repair (PLDR); heavy ion
Authors: Enriqueta Riballo; Martin Kühne; Nicole Rief; Aidan Doherty; Graeme C M Smith; María-José Recio; Caroline Reis; Kirsten Dahm; Andreas Fricke; Andrea Krempler; Antony R Parker; Stephen P Jackson; Andrew Gennery; Penny A Jeggo; Markus Löbrich Journal: Mol Cell Date: 2004-12-03 Impact factor: 17.970