Abstract
P-type transport ATPase’s are active transporters that dispense the majority of the cellular functions. ATP13A2 have a role in neurodegeneration which is commonly associated with lysosomal dysfunction. Lysosome plays a significant role in the metabolism, secretion, signaling, plasma membrane repair, and autophagy which have fundamental implications in different carcinomas. ATP13A2 is placed in the lysosome and the late endosome and the drastic dysfunction in the lysosome is caused from its mutation. However, this systematic study was done to evaluate ATP13A2 as the possible prognostic marker for the glioblastoma multiform (GBM) is the utmost frequent primary cancer of the central nervous system. Within this cumulative study, we have inspected the pattern of expression of ATP13A2 and their corresponding outcome in GBM patients using different available databases. We examined a comparative study of ATP13A2 expression between the normal tissues and their cancers using the UALCAN, Oncomine, GEPIA2, and GENT2 databases. Both analyses showed significantly high ATP13A2 mRNA and protein expression in GBM than those of normal tissues. We investigate clinicopathological expression and methylation characteristics of GBM using UALCAN database, which analysis showed clinicopathological expression of ATP13A2 was down regulated and methylation was over-expressed in GBM compared to normal tissues. We also investigate mutations and the alterations of copy number of ATP13A2 using a database called cBioPortal, which showing about 5 (0.2%) alteration and 0.6% mutation frequency and co-expression profile through the Oncomine. We used the Enricher tool to predict the signaling pathways in GBM through gene ontology and pathway analysis of co-expressed genes. The PrognoScan analysis revealed that the increased ATP13A2 expression correlates with worse patient survival. Finally, our derived data apprises that, ATP13A2 may serve as a potential biomarker of GBM/brain cancer patients.
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