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.
[1]Jilin Univ, Hosp 1, Dept Radiat Oncol, Changchun, Peoples R China.
[2]Emory Univ, Sch Med, Dept Radiat Oncol, 1365 Clifton Rd NE Suite 5090, Atlanta, GA 30322 USA.
[3]Emory Univ, Winship Canc Inst, 1365 Clifton Rd NE Suite 5090, Atlanta, GA 30322 USA.
(8.0+极速模式)