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无标记定量蛋白质组学揭示了极光激酶B在肾细胞癌中的作用机制。

Label-free quantitative proteomics reveals the mechanisms of Aurora kinase B in renal cell carcinoma.

作者信息

Li Yulong, Yang Yang

机构信息

Department of Gastroenterology, Shaanxi Provincial People's Hospital, Xi'an, China.

School of Public Health, Shaanxi University of Chinese Medicine, Xianyang, China.

出版信息

SAGE Open Med. 2024 Mar 20;12:20503121241228474. doi: 10.1177/20503121241228474. eCollection 2024.

DOI:10.1177/20503121241228474
PMID:38516642
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10956137/
Abstract

BACKGROUND

Renal cell carcinoma is the most common form of kidney cancer which is a global threat to human health, needing to explore effective therapeutic targets and treatment methods. Aurora kinase B acts as an important carcinogenic role in various kinds of tumors, while its mechanism in renal cell carcinoma is indistinct. Herein we explore the underlying mechanism of Aurora kinase B in renal cell carcinoma.

METHODS AND RESULTS

Label-free quantitative proteomics analysis was employed to analyze the differentially expressed proteins in 786-O cells which were treated with si-Aurora kinase B or si-ctrl. In the current study, 169 differentially expressed proteins were identified. The top 10 upregulated proteins were MX2, IFI44L, ISG20, DDX58, F3, IFI44, ECE1, PRIC285, NIT1, and IFIT2. The top 10 downregulated proteins were FKBP9, FSTL1, DDAH1, TGFB2, HMGN3, COIL, FAM65A, PTPN14, ARFGAP2, and EIF2C2. GO enrichment analysis showed that these differentially expressed proteins participated in biological processes, including defense response to virus, response to virus, and type I interferon signaling pathway. These differentially expressed proteins participated in cellular components, including focal adhesion, cell-substrate adherens junction, cell-substrate junction, and endoplasmic reticulum lumen. These differentially expressed proteins participated in molecule functions, including guanyl nucleotide binding, nucleotidase activity, double-stranded RNA binding, 2'-5'-oligoadenylate synthetase activity, and virus receptor activity. Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that the significantly changed proteins including OAS3, OAS2, JAK1, TAP1, and RAC1 were involved in Epstein-Barr virus infection.

CONCLUSIONS

Taken together, our results demonstrate the possible mechanisms that Aurora kinase B may participate in renal cell carcinoma. These findings may provide insights into tumorigenesis and a theoretical basis for developing potential therapies of renal cell carcinoma.

摘要

背景

肾细胞癌是最常见的肾癌形式,对人类健康构成全球威胁,需要探索有效的治疗靶点和治疗方法。极光激酶B在各种肿瘤中发挥重要的致癌作用,但其在肾细胞癌中的机制尚不清楚。在此,我们探讨极光激酶B在肾细胞癌中的潜在机制。

方法与结果

采用无标记定量蛋白质组学分析方法,分析用si-极光激酶B或si-对照处理的786-O细胞中差异表达的蛋白质。在本研究中,鉴定出169种差异表达的蛋白质。上调排名前十的蛋白质为MX2、IFI44L、ISG20、DDX58、F3、IFI44、ECE1、PRIC285、NIT1和IFIT2。下调排名前十的蛋白质为FKBP9、FSTL1、DDAH1、TGFB2、HMGN3、COIL、FAM65A、PTPN14、ARFGAP2和EIF2C2。基因本体富集分析表明,这些差异表达的蛋白质参与生物过程,包括对病毒的防御反应、对病毒的反应和I型干扰素信号通路。这些差异表达的蛋白质参与细胞成分,包括粘着斑、细胞-基质粘附连接、细胞-基质连接和内质网腔。这些差异表达的蛋白质参与分子功能,包括鸟苷核苷酸结合、核苷酸酶活性、双链RNA结合、2'-5'-寡腺苷酸合成酶活性和病毒受体活性。京都基因与基因组百科全书通路分析表明,包括OAS3、OAS2、JAK1、TAP1和RAC1在内的显著变化的蛋白质参与了爱泼斯坦-巴尔病毒感染。

结论

综上所述,我们的结果证明了极光激酶B可能参与肾细胞癌的潜在机制。这些发现可能为肿瘤发生提供见解,并为开发肾细胞癌的潜在治疗方法提供理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/312a/10956137/d27689d03d17/10.1177_20503121241228474-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/312a/10956137/360b1bcaa66e/10.1177_20503121241228474-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/312a/10956137/b1dbd5c78e52/10.1177_20503121241228474-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/312a/10956137/b869a53fe7b9/10.1177_20503121241228474-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/312a/10956137/d27689d03d17/10.1177_20503121241228474-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/312a/10956137/360b1bcaa66e/10.1177_20503121241228474-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/312a/10956137/b1dbd5c78e52/10.1177_20503121241228474-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/312a/10956137/b869a53fe7b9/10.1177_20503121241228474-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/312a/10956137/d27689d03d17/10.1177_20503121241228474-fig4.jpg

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