Investigation of JNK/Beclin-1 Autophagy Activation in SapC-DOPS Treated Glioma
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Publisher:The Ohio State University
Series/Report no.:The Ohio State University. School of Biomedical Science Honors Theses; 2013
Glioblastoma (GB) is a highly aggressive brain cancer that results in poor prognosis for afflicted patients. Saposin C-dioleoylphosphatidylserine (SapC-DOPS) nanovesicle is a novel therapeutic that has been shown to cross the blood brain barrier to target glioma tumors, activate acid sphingomyelinase, induce cell death, and improve survival of mice implanted with glioma xenografts. Histological investigation of the xenograft tumors demonstrates SapC-DOPS targets the tumor vasculature and selectively induces cell death within the tumor. Co-immunoprecipitation of GB neurospheres suggests the Beclin-1/Bcl-2 interaction is involved in SapC-DOPS induced cell death. Protein analysis of SapC-DOPS treated glioma cell lines suggests autophagy is activated through lipidation of LC3-I to active LC3-II and upstream activation of JNK1 may be involved. This study evaluates the in vivo effects of SapC-DOPS and elucidates a possible autophagy mechanism associated with glioma cell death. Further investigation of the induced cell death pathways is required to determine the main contributors to the SapC-DOPS induced glioma cell death with the hope of forming a combination therapy that enhances SapC-DOPS efficacy and improve prognosis for glioma brain tumor patients.
Related Item:Academic Major: Biomedical Science
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