Abstract
Glioblastomas are known to the most lethal brain tumor and their resistance to anti-cancer therapies is elucidated by glioma stem cells (GSC). But it is still unclear how the molecular mechanisms provide the resistance to GSCs. In this study, we used GSCs characterized by Plagl1, which is a tumorigenesis factor, and Sox11, which is the negative regulator of Plagl1. We compared the cellular characteristics between GSCs (Plagl1 positive) and glioma differentiated cells (Sox11 positive) by using anti-cancer drugs and ionizing radiations. In consequence, we found that GSCs showed stronger resistance to DNA cross-link agents whose damages are repaired by homologous recombination (HR), delay of IR-induced DNA damage foci's decreasing, rapid escape from cell cycle arrest and repression of apoptosis. These results might suggest that HR repair is induced in GSCs and therefore this increases cellular survivability and tumor malignancy.
