Sensitization of cancer cells to DNA damage-induced cell death by specific cell cycle G2 checkpoint abrogation.
basic_science · Level V
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Abstract
We devised two short peptides corresponding to amino acids 211-221 of human Cdc25C fused with a part of HIV1-TAT. These peptides inhibited hChk1 and Chk2/HuCds1 kinase activity in vitro and specifically abrogated the G2 checkpoint in vivo. These peptides sensitized p53-defective cancer cell lines to DNA-damaging agent to death without obvious cytotoxic effect on normal cells. Our results clearly indicate that the specific abrogation of the cell cycle G2 checkpoint is a feasible strategy for cancer therapy, and hChk1 and Chk2/HuCds1 are proper targets for that purpose.
Medical subject headings
- Cell Cycle
- Cell Cycle Proteins
- Cell Survival
- DNA Damage
- Gene Products, tat
- Peptide Fragments
- Recombinant Fusion Proteins
- cdc25 Phosphatases