Zhiliang Xiao , Yuan Wang , Dehua Pan , Xin Liu , Jin Gan , Liang Huang , Yan Feng
{"title":"USP3通过稳定MYC和促进糖酵解促进透明细胞肾细胞癌的进展","authors":"Zhiliang Xiao , Yuan Wang , Dehua Pan , Xin Liu , Jin Gan , Liang Huang , Yan Feng","doi":"10.1016/j.bbagen.2025.130801","DOIUrl":null,"url":null,"abstract":"<div><div>Clear cell renal cell carcinoma (ccRCC) is the most prevalent type of renal malignancy, and the deubiquitinase USP3 has been implicated as a critical factor in tumor biology. However, the precise mechanisms by which USP3 contributes to ccRCC progression remain unclear. This study investigates the role of USP3 in ccRCC and elucidates its underlying molecular mechanisms. Data from TCGA and GTEx databases showed elevated USP3 expression in ccRCC tissues and cell lines compared to normal renal tissues. Further analysis using qPCR and Western blot confirmed this upregulation in ccRCC cell lines. Functional assays revealed that silencing USP3 significantly impaired cell proliferation, migration, and invasion, while promoting apoptosis. Additionally, co-immunoprecipitation assays demonstrated an interaction between USP3 and MYC, with subsequent ubiquitination assays showing that USP3 regulates MYC stability. USP3 depletion also led to alterations in glycolysis-related gene expression, which could be partially reversed by MYC overexpression. These findings suggest that USP3 modulates ccRCC progression by stabilizing MYC, highlighting its potential as a therapeutic target in ccRCC treatment.</div></div>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":"1869 6","pages":"Article 130801"},"PeriodicalIF":2.8000,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"USP3 promotes clear cell renal cell carcinoma progression by stabilizing MYC and enhancing glycolysis\",\"authors\":\"Zhiliang Xiao , Yuan Wang , Dehua Pan , Xin Liu , Jin Gan , Liang Huang , Yan Feng\",\"doi\":\"10.1016/j.bbagen.2025.130801\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Clear cell renal cell carcinoma (ccRCC) is the most prevalent type of renal malignancy, and the deubiquitinase USP3 has been implicated as a critical factor in tumor biology. However, the precise mechanisms by which USP3 contributes to ccRCC progression remain unclear. This study investigates the role of USP3 in ccRCC and elucidates its underlying molecular mechanisms. Data from TCGA and GTEx databases showed elevated USP3 expression in ccRCC tissues and cell lines compared to normal renal tissues. Further analysis using qPCR and Western blot confirmed this upregulation in ccRCC cell lines. Functional assays revealed that silencing USP3 significantly impaired cell proliferation, migration, and invasion, while promoting apoptosis. Additionally, co-immunoprecipitation assays demonstrated an interaction between USP3 and MYC, with subsequent ubiquitination assays showing that USP3 regulates MYC stability. USP3 depletion also led to alterations in glycolysis-related gene expression, which could be partially reversed by MYC overexpression. These findings suggest that USP3 modulates ccRCC progression by stabilizing MYC, highlighting its potential as a therapeutic target in ccRCC treatment.</div></div>\",\"PeriodicalId\":8800,\"journal\":{\"name\":\"Biochimica et biophysica acta. General subjects\",\"volume\":\"1869 6\",\"pages\":\"Article 130801\"},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2025-03-29\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biochimica et biophysica acta. General subjects\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0304416525000467\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochimica et biophysica acta. General subjects","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0304416525000467","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
USP3 promotes clear cell renal cell carcinoma progression by stabilizing MYC and enhancing glycolysis
Clear cell renal cell carcinoma (ccRCC) is the most prevalent type of renal malignancy, and the deubiquitinase USP3 has been implicated as a critical factor in tumor biology. However, the precise mechanisms by which USP3 contributes to ccRCC progression remain unclear. This study investigates the role of USP3 in ccRCC and elucidates its underlying molecular mechanisms. Data from TCGA and GTEx databases showed elevated USP3 expression in ccRCC tissues and cell lines compared to normal renal tissues. Further analysis using qPCR and Western blot confirmed this upregulation in ccRCC cell lines. Functional assays revealed that silencing USP3 significantly impaired cell proliferation, migration, and invasion, while promoting apoptosis. Additionally, co-immunoprecipitation assays demonstrated an interaction between USP3 and MYC, with subsequent ubiquitination assays showing that USP3 regulates MYC stability. USP3 depletion also led to alterations in glycolysis-related gene expression, which could be partially reversed by MYC overexpression. These findings suggest that USP3 modulates ccRCC progression by stabilizing MYC, highlighting its potential as a therapeutic target in ccRCC treatment.
期刊介绍:
BBA General Subjects accepts for submission either original, hypothesis-driven studies or reviews covering subjects in biochemistry and biophysics that are considered to have general interest for a wide audience. Manuscripts with interdisciplinary approaches are especially encouraged.