Tumor Biol. DOI 10.1007/s13277-013-1465-9
RESEARCH ARTICLE
The influence of AKT isoforms on radiation sensitivity and DNA repair in colon cancer cell lines Sara Häggblad Sahlberg & Ann-Sofie Gustafsson & Prathyusha N. Pendekanti & Bengt Glimelius & Bo Stenerlöw
Received: 1 October 2013 / Accepted: 22 November 2013 # The Author(s) 2013. This article is published with open access at Springerlink.com
Abstract In response to ionizing radiation, several signaling cascades in the cell are activated to repair the DNA breaks, prevent apoptosis, and keep the cells proliferating. AKT is important for survival and proliferation and may also be an activating factor for DNA-PKcs and MRE11, which are essential proteins in the DNA repair process. AKT (PKB) is hyperactivated in several cancers and is associated with resistance to radiotherapy and chemotherapy. There are three AKT isoforms (AKT1, AKT2, and AKT3) with different expression patterns and functions in several cancer tumors. The role of AKT isoforms has been investigated in relation to radiation response and their effects on DNA repair proteins (DNAPKcs and MRE11) in colon cancer cell lines. The knockout of AKT1 and/or AKT2 affected the radiation sensitivity, and a deficiency of both isoforms impaired the rejoining of radiation-induced DNA double strand breaks. Importantly, the active/phosphorylated forms of AKT and DNA-PKcs Electronic supplementary material The online version of this article (doi:10.1007/s13277-013-1465-9) contains supplementary material, which is available to authorized users. S. H. Sahlberg (*) : A.
RESEARCH ARTICLE
The influence of AKT isoforms on radiation sensitivity and DNA repair in colon cancer cell lines Sara Häggblad Sahlberg & Ann-Sofie Gustafsson & Prathyusha N. Pendekanti & Bengt Glimelius & Bo Stenerlöw
Received: 1 October 2013 / Accepted: 22 November 2013 # The Author(s) 2013. This article is published with open access at Springerlink.com
Abstract In response to ionizing radiation, several signaling cascades in the cell are activated to repair the DNA breaks, prevent apoptosis, and keep the cells proliferating. AKT is important for survival and proliferation and may also be an activating factor for DNA-PKcs and MRE11, which are essential proteins in the DNA repair process. AKT (PKB) is hyperactivated in several cancers and is associated with resistance to radiotherapy and chemotherapy. There are three AKT isoforms (AKT1, AKT2, and AKT3) with different expression patterns and functions in several cancer tumors. The role of AKT isoforms has been investigated in relation to radiation response and their effects on DNA repair proteins (DNAPKcs and MRE11) in colon cancer cell lines. The knockout of AKT1 and/or AKT2 affected the radiation sensitivity, and a deficiency of both isoforms impaired the rejoining of radiation-induced DNA double strand breaks. Importantly, the active/phosphorylated forms of AKT and DNA-PKcs Electronic supplementary material The online version of this article (doi:10.1007/s13277-013-1465-9) contains supplementary material, which is available to authorized users. S. H. Sahlberg (*) : A.
