DNA-PK, a Pharmacological Target in Cancer Chemotherapy and Radiotherapy?
- *Corresponding Author:
- Bernard Salles
DVM, PhD, INRA, Université de Toulouse
III, UMR1331, Toxalim (Research Centre in Food Toxicology)
F-31027 Toulouse, France
E-mail: [email protected]
Received Date: October 17, 2011; Accepted Date: December 01, 2011; Published Date: December 03, 2011
Citation: Salles B, Calsou P, Mirey G (2011) DNA-PK, a Pharmacological Target in Cancer Chemotherapy and Radiotherapy? J Cancer Sci Ther S8:001. doi:10.4172/1948-5956.S8-001
Copyright: © 2011 Salles B, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
In the search for ways of sensitizing tumor cells to chemotherapy or radiotherapy, the inhibition of DNA repair has recently been proposed as a target of clinical interest. Ionizing radiation, as well as several antitumor drugs, induce the formation of DNA double-strand breaks (DSBs), that are highly damaging to the DNA, leading to cell death and genomic instability. DSBs are mainly repaired by the Non-Homologous End-Joining (NHEJ) process, in which DNA dependent protein kinase (DNA-PK) is the key complex. Consequently, specific DNA-PK inhibitors have been selected and evaluated for sensitizing cells to chemotherapy or radiotherapy. The choice of DNA-PK as a pharmacological target of interest in cancer treatment is discussed.