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

IF 1.6 4区 医学 Q4 ONCOLOGY
Jaber H Jaradat, Yassine Alami Idrissi, Anwaar Saeed
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引用次数: 0

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.

HOOK3在膀胱尿路上皮癌中的扩增:来自基因表达和生存分析的见解。
背景/目的:膀胱尿路上皮癌(BUC)是一个重大的健康挑战,是美国男性第四大常见癌症,死亡率约为20%。遗传异常,如端粒酶逆转录酶(TERT)基因突变和9号染色体杂合性缺失(LOH)在BUC中很常见;然而,许多相关基因仍未被识别。本研究旨在探讨HOOK3在BUC中的作用及其对生存的影响。材料和方法:利用癌症基因组图谱(TCGA)和cbiopportal的数据,我们进行了差异基因表达和生存分析,比较了HOOK3扩增和未扩增的患者。结果:我们的研究结果显示,在hook3扩增组中,2.2%的基因上调,5.3%的基因下调。这些变化表明,HOOK3扩增与不同的基因表达模式有关,其中下调基因的比例较高。与染色质重塑、离子转运和线粒体功能相关的通路富集表明,HOOK3可能促进基因组稳定性和转录调控,有助于抑制肿瘤。参与蛋白质合成和染色体分离的线粒体和核糖体途径也可能防止染色体异常和不受控制的细胞生长。HOOK3扩增似乎与患者生存率的提高有关。结论:这些结果提示HOOK3扩增对BUC具有潜在的保护作用。需要进一步的研究来探索其潜在的机制及其降低bucc相关死亡率的治疗潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Anticancer research
Anticancer research 医学-肿瘤学
CiteScore
3.70
自引率
10.00%
发文量
566
审稿时长
2 months
期刊介绍: ANTICANCER RESEARCH is an independent international peer-reviewed journal devoted to the rapid publication of high quality original articles and reviews on all aspects of experimental and clinical oncology. Prompt evaluation of all submitted articles in confidence and rapid publication within 1-2 months of acceptance are guaranteed. ANTICANCER RESEARCH was established in 1981 and is published monthly (bimonthly until the end of 2008). Each annual volume contains twelve issues and index. Each issue may be divided into three parts (A: Reviews, B: Experimental studies, and C: Clinical and Epidemiological studies). Special issues, presenting the proceedings of meetings or groups of papers on topics of significant progress, will also be included in each volume. There is no limitation to the number of pages per issue.
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