DNA-dependent protein kinase regulated glioblastoma survival in doxorubicin-induced cytotoxicity

Generally, chemotherapy is effective when the cancer cell is dividing; most drugs trigger cancer cells to undergo apoptosis by attacking the cell’s DNA. In the process of cancer cell apoptosis, cancer cells become more resistant to chemotherapy treatments over time. Since DNA-dependent protein kinase (DNA-PK) plays an important role in DNA repairing, it is interesting to investigate the relationship between this particular enzyme and the development of multidrug resistance. In this study, we chose the commonly used chemotherapy drug doxorubicin to treat glioblastoma cells (M059k and M059j), and performed 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenykterazolium bromide (MTT) assay and immunofluorescence staining to assess the presence of DNA-PK. The result of MTT assay showed that the concentration of an inhibitor/drug required to reduce the cell viability by half of M059j is 1.75 μm while that of M059k is 0.71 μm after doxorubicin treatment. Comparing the staining result of M059j and M059k, DNA-PK was more detectable in M059k than in M059j. It suggested that further experiments need to be performed to identify and characterize the proteins that are important for signal transduction pathways that actually link DNA-PK with doxorubicin-induced cytotoxicity as well as those that are drug resistant.