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Differential expression analysis of lysosomal storage related genes in gliomas

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Introduction: Defects in activity and transport of lysosomal hydrolases lead to the accumulation of lysosomal metabolites, causing lysosomal storage disease (LSD). The involvement of lysosomes also has been described in tumors, related to cell proliferation and signaling processes, microbial killing, cytotoxic killing, induction of angiogenesis, cell adhesion and metastatic processes. Aims: This work aims to investigate the differential expression of lysosomal genes and autophagy-related genes in brain tumors. Data from patients with different brain tumors were collected and analyzed through the R2: Genomics Analysis and Visualization Platform. Gene expression analysis was performed on 50 gliomas with five pathological diagnosis. Sample tracks were divided in recurrence of progression and description of the tumor. All differentially expressed genes were correlated with survival rates using Kaplan Meier. Results: From 113 selected genes (KEGG pathway: lysosome), 24 were up-regulated and 6 were down-regulated. Heatmap analysis showed that 30 genes have a distinct pattern for grade IV glioblastoma multiforme. Survival analysis showed that cathepsin expression correlates with poor survival, as previously shown for other tumors. In addition, similar results were found for different lysosomal hydrolases, such as Beta-Manosidase, Galactosidase, Glucorunidase beta, and, Hexosaminidase, and autophagy-related genes. Conclusion: Studying the lysosomal signature in tumors may help understand the mechanisms by which neurological dysfunction occurs both in patients with neurological tumors and in patients with lysosomal storage diseases. Besides, differentially expressed genes may serve as prognostic biomarkers and therapeutic targets. Also, may improve diagnosis and lead patients to a more adequate treatment.
Title: Differential expression analysis of lysosomal storage related genes in gliomas
Description:
Introduction: Defects in activity and transport of lysosomal hydrolases lead to the accumulation of lysosomal metabolites, causing lysosomal storage disease (LSD).
The involvement of lysosomes also has been described in tumors, related to cell proliferation and signaling processes, microbial killing, cytotoxic killing, induction of angiogenesis, cell adhesion and metastatic processes.
Aims: This work aims to investigate the differential expression of lysosomal genes and autophagy-related genes in brain tumors.
Data from patients with different brain tumors were collected and analyzed through the R2: Genomics Analysis and Visualization Platform.
Gene expression analysis was performed on 50 gliomas with five pathological diagnosis.
Sample tracks were divided in recurrence of progression and description of the tumor.
All differentially expressed genes were correlated with survival rates using Kaplan Meier.
Results: From 113 selected genes (KEGG pathway: lysosome), 24 were up-regulated and 6 were down-regulated.
Heatmap analysis showed that 30 genes have a distinct pattern for grade IV glioblastoma multiforme.
Survival analysis showed that cathepsin expression correlates with poor survival, as previously shown for other tumors.
In addition, similar results were found for different lysosomal hydrolases, such as Beta-Manosidase, Galactosidase, Glucorunidase beta, and, Hexosaminidase, and autophagy-related genes.
Conclusion: Studying the lysosomal signature in tumors may help understand the mechanisms by which neurological dysfunction occurs both in patients with neurological tumors and in patients with lysosomal storage diseases.
Besides, differentially expressed genes may serve as prognostic biomarkers and therapeutic targets.
Also, may improve diagnosis and lead patients to a more adequate treatment.

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