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Glioblastoma multiforme is one of the deadliest forms of brain tumor with a median survival of <12 months with a high rate of recurrence. Glioblastoma cells respond poorly to radiother‐ apy and chemotherapy due to elevated DNA repair efficiency coupled with anti-apoptotic mechanisms [1, 2]. Therefore, development of new therapeutic strategies is absolutely critical either to control or cure the disease. Since glioblastoma cells have inherently elevated levels of DNA damage response (DDR) and DNA repair efficiency, we sought to determine whether or not suppression of key DNA repair factor(s) might be effective in sensitizing the brain tumor cells to chemotherapy. To test our objective, a pair of isogenic glioblastoma cell lines that differ in the functional status of DNA dependent protein kinase (DNA-PK) has been chosen. DNA dependent protein kinase (DNA-PK) belongs to a super family of phosphatidylinositol-3 kinase like kinases (PIKK) which also includes the gene products of ataxia telangiectasia mutated (ATM) and ATM and Rad 3 related (ATR) kinases [3, 4]. DNA-PK is the main component of mammalian NHEJ (non-homologous end joining), and also plays a role as a sensor of DNA damage by phosphorylating several downstream targets [5]. Further, DNAPK has been demonstrated to be an important component of nucleotide excision repair (NER) pathway, which is chiefly responsible for the repair of bulky and helix distorting lesions induced by ultraviolet radiation (UV) and chemotherapeutic drugs such as cisplatin. To determine whether or not DNA-PK is a potential molecular therapeutic target for glioblastoma, two agents with different modes of action have been chosen for our study: (1) Zebularine and (2) Cisplatin.

DNA-PK is a Potential Molecular Therapeutic Target for Glioblastoma