BUD31 在透明细胞肾细胞癌中的作用:预后意义、替代剪接和肿瘤免疫环境。

IF 3.2 4区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL
Xiaoliang Wu, Ruixin Fan, Yangjun Zhang, Chen Duan, Xiangyang Yao, Kai Liu, Dongxu Lin, Zhong Chen
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引用次数: 0

摘要

BUD31 是一种剪接因子,与多种癌症有关。本研究探讨了 BUD31 的表达、预后价值、突变情况、基因组不稳定性、肿瘤免疫环境以及在透明细胞肾细胞癌(ccRCC)中的作用,重点是通过替代剪接调节细胞周期。利用 TCGA 和 GTEx 数据库分析了 33 种癌症中 BUD31 的表达情况。分析技术包括 IHC 染色、生存分析、Cox 回归和构建提名图。对突变情况、基因组不稳定性和肿瘤免疫微环境进行了评估。ccRCC细胞系的功能测试包括BUD31基因敲除、RNA测序和替代剪接分析。BUD31在多种肿瘤(包括ccRCC)中上调。BUD31 的高表达与较差的生存结果相关,并被确定为 ccRCC 预后不良的独立预测因子。BUD31 的高表达还与基因组不稳定性增加和免疫微环境不活跃有关。BUD31 基因敲除抑制了体外的细胞增殖、迁移和侵袭,并降低了体内的肿瘤生长。RNA测序发现了390个受BUD31调控的替代剪接事件,包括17个细胞周期相关基因。KEGG分析强调了参与细胞周期调控的通路,表明BUD31在通过替代剪接促进细胞周期进展方面的作用。BUD31在多种肿瘤中上调,与ccRCC的不良预后、基因组不稳定性增加和免疫微环境抑制有关。BUD31通过替代剪接促进细胞周期进展,这表明它是ccRCC的预后生物标志物和潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The role of BUD31 in clear cell renal cell carcinoma: prognostic significance, alternative splicing, and tumor immune environment.

The role of BUD31 in clear cell renal cell carcinoma: prognostic significance, alternative splicing, and tumor immune environment.

BUD31, a splicing factor, is linked to various cancers. This study examines BUD31's expression, prognostic value, mutation profile, genomic instability, tumor immune environment, and role in clear cell renal cell carcinoma (ccRCC), focusing on cell cycle regulation via alternative splicing. BUD31 expression was analyzed using TCGA and GTEx databases across 33 cancers. Techniques included IHC staining, survival analysis, Cox regression, and nomogram construction. Mutation landscape, genomic instability, and tumor immune microenvironment were evaluated. Functional assays on ccRCC cell lines involved BUD31 knockdown, RNA sequencing, and alternative splicing analysis. BUD31 was upregulated in multiple tumors, including ccRCC. High BUD31 expression correlated with worse survival outcomes and was identified as an independent predictor of poor prognosis in ccRCC. High BUD31 expression also correlated with increased genomic instability and a less active immune microenvironment. BUD31 knockdown inhibited cell proliferation, migration, and invasion in vitro and reduced tumor growth in vivo. RNA sequencing identified 390 alternative splicing events regulated by BUD31, including 17 cell cycle-related genes. KEGG analysis highlighted pathways involved in cell cycle regulation, indicating BUD31's role in promoting cell cycle progression through alternative splicing. BUD31 is upregulated in various tumors and is associated with poor outcomes, increased genomic instability, and a suppressed immune microenvironment in ccRCC. BUD31 promotes cell cycle progression via alternative splicing, suggesting it as a prognostic biomarker and potential therapeutic target in ccRCC.

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来源期刊
Clinical and Experimental Medicine
Clinical and Experimental Medicine 医学-医学:研究与实验
CiteScore
4.80
自引率
2.20%
发文量
159
审稿时长
2.5 months
期刊介绍: Clinical and Experimental Medicine (CEM) is a multidisciplinary journal that aims to be a forum of scientific excellence and information exchange in relation to the basic and clinical features of the following fields: hematology, onco-hematology, oncology, virology, immunology, and rheumatology. The journal publishes reviews and editorials, experimental and preclinical studies, translational research, prospectively designed clinical trials, and epidemiological studies. Papers containing new clinical or experimental data that are likely to contribute to changes in clinical practice or the way in which a disease is thought about will be given priority due to their immediate importance. Case reports will be accepted on an exceptional basis only, and their submission is discouraged. The major criteria for publication are clarity, scientific soundness, and advances in knowledge. In compliance with the overwhelmingly prevailing request by the international scientific community, and with respect for eco-compatibility issues, CEM is now published exclusively online.
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