ArticleProceedings of the National Academy of Sciences of the United States of America2020
USP37 promotes deubiquitination of HIF2α in kidney cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 56 citations in OpenAlex.
- Deubiquitinating enzymes in kidney diseases: Molecular mechanisms, pathological roles and therapeutic opportunities (Review).Molecular medicine reports · 2026Review
- ACSL3 inhibits ferroptosis in gastric cancer through the activation of unfolded protein response following endoplasmic reticulum stress.Cell death & disease · 2026Article
- USP37 facilitates hepatocellular carcinoma progression by deubiquitinating RAF1 and activating ERK1/2 signaling.Functional & integrative genomics · 2026Article
- USP52 promotes clear cell renal carcinoma progression by deubiquitinating and stabilizing CORO6.Translational oncology · 2026Article
- USP48 promotes tumour progression through the deubiquitination and stabilization of DBF4 in clear cell renal carcinoma.Cancer cell international · 2026Article
- USP18 promotes clear cell renal cell carcinoma progression by regulating the ubiquitination and stability of YBX3.iScience · 2026Article
- USP10 regulates HIF2α stability by deubiquitinating HIF2α regardless ofTranslational andrology and urology · 2026Article
- Identification of Raptor and GLI1 as USP37 substrates highlight its context-specific function in medulloblastoma cells.Oncogene · 2026Article
- Clinicopathological significance and exploratory prognostic modeling of USP18 and YBX3 expression in clear cell renal cell carcinoma: a retrospective Chinese cohort study.Frontiers in oncology · 2026Article
- OTUD1 downregulates PD-L1 expression by deubiquitinating STAT3 and promotes the immune response in ccRCC.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- USP39 promote post-translational modifiers to stimulate the progress of cancer.Discover oncology · 2025Review
- Loss of VHL-mediated pRb regulation promotes clear cell renal cell carcinoma.Cell death & disease · 2025Article
- Oncogenic and immunological functions of USP35 in pan-cancer and its potential as a biomarker in kidney clear cell carcinoma.BMC cancer · 2025Article
- CDK1-mediated phosphorylation of USP37 regulates SND1 stability and promotes oncogenesis in colorectal cancer.Acta pharmaceutica Sinica. B · 2025Article
- Article
- Clear cell renal carcinoma essentially requires CDKL3 for oncogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- HIF2α drives ccRCC metastasis through transcriptional activation of methylation-controlled J protein and enhanced prolegumain secretion.Cell death & disease · 2025Article
- Deubiquitinase USP37 enhances the anti-HIV-2/SIV ability of the host restriction factor SAMHD1.Journal of virology · 2025Article
- Roles of E3 ubiquitin ligases and deubiquitinating enzymes in renal cell carcinoma.Frontiers in oncology · 2025Review
- An integrative pan-cancer analysis of USP37 and functional validation in pancreatic cancer.Frontiers in cell and developmental biology · 2025Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Clear cell renal cell carcinoma (ccRCC) is characterized by loss of tumor suppressor Von Hippel Lindau (VHL) function, which leads to accumulation of hypoxia inducible factor α (including HIF1α and HIF2α). HIF2α was previously reported to be one of the major oncogenic drivers in ccRCC, however, its therapeutic targets remain challenging. Here we performed a deubiquitinase (DUB) complementary DNA (cDNA) library binding screen and discovered that ubiquitin-specific peptidase 37 (USP37) is a DUB that binds HIF2α and promotes HIF2α deubiquitination. As a result, USP37 promotes HIF2α protein stability in an enzymatically dependent manner, and depletion of USP37 leads to HIF2α down-regulation in ccRCC. Functionally, USP37 depletion causes decreased cell proliferation measured by MTS, two-dimensional (2D) colony formation as well as three-dimensional (3D) anchorage- independent growth. USP37 is also essential for maintaining kidney tumorigenesis in an orthotopic xenograft model and its depletion leads to both decreased primary kidney tumorigenesis and spontaneous lung metastasis. Our results suggest that USP37 is a potential therapeutic target in ccRCC.
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