HOOK3 Amplification in Bladder Urothelial Carcinoma: Insights from Gene Expression and Survival Analysis.

Anticancer Res

Department of Medicine, Division of Hematology & Oncology, University of Pittsburgh Medical Center, Pittsburgh, PA, U.S.A.;

Published: December 2024

AI Article Synopsis

  • * This study analyzed data from The Cancer Genome Atlas to investigate the effects of HOOK3 gene amplification on gene expression and patient survival in BUC, finding that HOOK3 amplification is associated with distinct gene changes and potential tumor suppression mechanisms.
  • * The results suggest that HOOK3 amplification may improve survival rates in BUC patients, indicating a protective role; however, more research is necessary to fully understand its mechanisms and therapeutic potential.

Article Abstract

Background/aim: Bladder urothelial carcinoma (BUC) poses a significant health challenge, ranking as the fourth most common cancer among men in the United States, with a mortality rate of approximately 20%. Genetic abnormalities such as mutations in the telomerase reverse transcriptase (TERT) gene and loss of heterozygosity (LOH) on chromosome 9 are commonly observed in BUC; however, many genes involved remain unidentified. This study aimed to explore the role of HOOK3 in BUC and its impact on survival.

Materials And Methods: Using data from The Cancer Genome Atlas (TCGA) and cBioPortal, we performed differential gene expression and survival analyses to compare the patients with and without HOOK3 amplification.

Results: Our findings revealed that 2.2% of genes were up-regulated and 5.3% down-regulated in the HOOK3-amplified group. These changes suggest that HOOK3 amplification is linked to distinct gene expression patterns, with a higher proportion of down-regulated genes. Pathway enrichment related to chromatin remodeling, ion transport, and mitochondrial function suggests that HOOK3 may promote genomic stability and transcriptional regulation, contributing to tumor suppression. The involvement of mitochondrial and ribosomal pathways in protein synthesis and chromosome segregation may also protect against chromosomal abnormalities and uncontrolled cell growth. HOOK3 amplification appears to correlate with improved patient survival.

Conclusion: These results suggest a potential protective role of HOOK3 amplification in BUC. Further research is needed to explore the underlying mechanisms and their therapeutic potential for reducing BUC-related mortality.

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Source
http://dx.doi.org/10.21873/anticanres.17343DOI Listing

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  • * This study analyzed data from The Cancer Genome Atlas to investigate the effects of HOOK3 gene amplification on gene expression and patient survival in BUC, finding that HOOK3 amplification is associated with distinct gene changes and potential tumor suppression mechanisms.
  • * The results suggest that HOOK3 amplification may improve survival rates in BUC patients, indicating a protective role; however, more research is necessary to fully understand its mechanisms and therapeutic potential.
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