ArticleCell death & disease2019
USP22-dependent HSP90AB1 expression promotes resistance to HSP90 inhibition in mammary and colorectal cancer.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
- SIRT2-mediated deacetylation activates USP22 catalytic function for PD-L1 protein stabilization and tumor immune escape.The Journal of clinical investigation · 2026Article
- USP22 deubiquitinates and stabilizes ERK1/2 to promote colorectal cancer progression.Acta pharmacologica Sinica · 2026Article
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- RnaXtract, a tool for extracting gene expression, variants, and cell-type composition from bulk RNA sequencing.Scientific reports · 2025Article
- Hepatocyte growth factor promotes melanoma metastasis through ubiquitin-specific peptidase 22-mediated integrins upregulation.Cancer letters · 2024Article
- Ubiquitin-specific peptidase 22 controls integrin-dependent cancer cell stemness and metastasis.iScience · 2024Article
- The secoiridoid glycoside Gentiopicroside is a USP22 inhibitor with potent antitumor immunotherapeutic activity.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
- USP22 supports the aggressive behavior of basal-like breast cancer by stimulating cellular respiration.Cell communication and signaling : CCS · 2024Article
- Comprehensive analysis of the role of ubiquitin-specific peptidases in colorectal cancer: A systematic review.World journal of gastrointestinal oncology · 2024Article
- An Overview of the Deubiquitinase USP53: A Promising Diagnostic Marker and Therapeutic Target.Current protein & peptide science · 2024Review
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- USP22 overexpression fails to augment tumor formation in MMTV-ERBB2 mice but loss of function impacts MMTV promoter activity.PloS one · 2024Article
- Mapping the tumor microenvironment in clear cell renal carcinoma by single-cell transcriptome analysis.Frontiers in genetics · 2023Article
- Large-Scale Identification of Lysine Crotonylation Reveals Its Potential Role in Oral Squamous Cell Carcinoma.Cancer management and research · 2023Article
- USP22 controls type III interferon signaling and SARS-CoV-2 infection through activation of STING.Cell death & disease · 2022Article
- KAT2A complexes ATAC and SAGA play unique roles in cell maintenance and identity in hematopoiesis and leukemia.Blood advances · 2022Article
- Immune Evasion and Drug Resistance Mediated by USP22 in Cancer: Novel Targets and Mechanisms.Frontiers in immunology · 2022Review
- Chromatin Dynamics in Digestive System Cancer: Commander and Regulator.Frontiers in oncology · 2022Review
- HSP70 and HSP90 in Cancer: Cytosolic, Endoplasmic Reticulum and Mitochondrial Chaperones of Tumorigenesis.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a member of the 11-gene "death-from-cancer" gene expression signature, overexpression of the Ubiquitin-Specific Protease 22 (USP22) was associated with poor prognosis in various human malignancies. To investigate the function of USP22 in cancer development and progression, we sought to detect common USP22-dependent molecular mechanisms in human colorectal and breast cancer cell lines. We performed mRNA-seq to compare gene expression profiles of various colorectal (SW837, SW480, HCT116) and mammary (HCC1954 and MCF10A) cell lines upon siRNA-mediated knockdown of USP22. Intriguingly, while USP22 depletion had highly heterogeneous effects across the cell lines, all cell lines displayed a common reduction in the expression of Heat Shock Protein 90 Alpha Family Class B Member 1 (HSP90AB1). The downregulation of HSP90AB1 was confirmed at the protein level in these cell lines as well as in colorectal and mammary tumors in mice with tissue-specific Usp22 deletions. Mechanistically, we detected a significant reduction of H3K9ac on the HSP90AB1 gene in USP22-deficient cells. Interestingly, USP22-deficient cells displayed a high dependence on HSP90AB1 expression and diminishing HSP90 activity further using the HSP90 inhibitor Ganetespib resulted in increased therapeutic vulnerability in both colorectal and breast cancer cells in vitro. Accordingly, subcutaneously transplanted CRC cells deficient in USP22 expression displayed increased sensitivity towards Ganetespib treatment in vivo. Together, we discovered that HSP90AB1 is USP22-dependent and that cooperative targeting of USP22 and HSP90 may provide an effective approach to the treatment of colorectal and breast cancer.
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