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Dilara Akcora-Yildiz

Mehmet Akif Ersoy University, Turkey

Title: Increased expression of CD24 in Glioblastoma Cell Lines after treatment with Temozolomide and Bortezomib

Biography

Biography: Dilara Akcora-Yildiz

Abstract

Glioblastoma Multiforme (GBM), is the most prevalent and aggressive type of primary brain tumour with a median survival of only 15 months due to recurrence of tumour after surgical resection and acquisition of resistance to radiotherapy or chemotherapy. Temozolomide (TMZ) an oral alkylating agent leading to the occurrence of DNA damage has been still used for GBM treatment. Other than TMZ, Bortezomib (BZ), currently in clinical use for the treatment of myeloma by achieving proteasome inhibition, has been revealed to induce apoptosis and growth inhibition in GBM cells. Our purpose was to examine the role of potential cancer stem cell markers including CD133, CD38, CD24, CD70 and DR6 in cell survival after either TMZ or bortezomib treatment. U118 GBM cell line and other GBM cell lines including U87, U138 and T98 were incubated with TMZ and BZ for 48 hr, respectively.  Real Time Cancer Stem Cell, Integrin, Apoptosis and Cell Adhesion PCR Arrays (Bio-Rad) were performed in U118 cells treated with TMZ for 48 hr. Flow cytometry assay was used to determine the protein amounts of the genes of interest after BZ treatment. Treatment with TMZ led to an increase in mRNA expression of CD38 and CD24 but not in CD70 and DR6. BZ decreased the expression of CD133 and CD38, whereas CD24 expression was found to be increased in a dose-dependent manner in all GBM cell lines. Furthermore, CD70 protein expression was elevated, while DR6 protein expression was reduced with the increase of the dose of BZ. Our results suggest that CD24 seems to be involved in GBM cell survival after either TMZ or BZ treatment, indicating inhibition of its expression might benefit to overcome chemo resistance. This research has been supported by The Scientific and Technological Research Council of Turkey (No: 114S189).