ArticleCell death and differentiation2020
USP22 exerts tumor-suppressive functions in colorectal cancer by decreasing mTOR activity.
Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 66 citations in OpenAlex.
- Loss of the USP22 deubiquitylase confers resistance to chemotherapy in small cell lung cancer.Nature communications · 2026Article
- Decoding the Oncogenic Role of USP22 Through Pan-Cancer Genomic and Epigenetic Analysis.Cancer reports (Hoboken, N.J.) · 2026Article
- LncRNA TAF1A-AS1 regulates the progression in hepatocellular carcinoma by targeting miR-664b-3p/USP22 axis.Discover oncology · 2026Article
- Regulatory roles of five key USP family deubiquitinases in cancer: from mechanisms to targeted therapy advances.Frontiers in pharmacology · 2026Review
- Multidimensional analysis of deubiquitinating enzymes in colorectal cancer: biological mechanisms and targeted therapeutic strategies.Frontiers in oncology · 2026Review
- Immunoregulatory roles of post-translational modifications in colorectal cancer: mechanisms and therapeutic implications.Cellular and molecular life sciences : CMLS · 2025Review
- USP39 promote post-translational modifiers to stimulate the progress of cancer.Discover oncology · 2025Review
- Demethylzeylasteral induces PD-L1 ubiquitin-proteasome degradation and promotes antitumor immunityActa pharmaceutica Sinica. B · 2024Article
- The Deubiquitinase USP22-Stabilized COL17A1 Promotes Lung Adenocarcinoma Progression.The clinical respiratory journal · 2024Article
- EZH2 Inhibition Enhances PD-L1 Protein Stability Through USP22-Mediated Deubiquitination in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- High-Throughput Mass Spectrometry Analysis ofJournal of proteome research · 2024Article
- Ubiquitin-specific protease 21 promotes tumorigenicity and stemness of colorectal cancer by deubiquitinating and stabilizing ZEB1.World journal of gastrointestinal oncology · 2024Article
- AMPKα2 promotes tumor immune escape by inducing CD8+ T-cell exhaustion and CD4+ Treg cell formation in liver hepatocellular carcinoma.BMC cancer · 2024Article
- Comprehensive analysis of the role of ubiquitin-specific peptidases in colorectal cancer: A systematic review.World journal of gastrointestinal oncology · 2024Article
- USP22 overexpression fails to augment tumor formation in MMTV-ERBB2 mice but loss of function impacts MMTV promoter activity.PloS one · 2024Article
- Article
- Deubiquitinases in cancer.Nature reviews. Cancer · 2023Review
- Phosphorylation of USP27X by GSK3β maintains the stability and oncogenic functions of CBX2.Cell death & disease · 2023Article
- USP22 knockdown protects against cerebral ischemia/reperfusion injury via destabilizing PTEN protein and activating the mTOR/TFEB pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
USP22, the deubiquitinating subunit of the SAGA transcriptional cofactor complex, is a member of an 11-gene "death-from-cancer" signature. USP22 has been considered an attractive therapeutic target since high levels of its expression were associated with distant metastasis, poor survival, and high recurrence rates in a wide variety of solid tumors, including colorectal cancer (CRC). We sought to investigate the role of Usp22 during tumorigenesis in vivo using a mouse model for intestinal carcinogenesis with a tissue-specific Usp22 ablation. In addition, we assessed the effects of USP22 depletion in human CRC cells on tumorigenic potential and identified underlying molecular mechanisms. For the first time, we report that USP22 has an unexpected tumor-suppressive function in vivo. Intriguingly, intestine-specific Usp22 deletion exacerbated the tumor phenotype caused by Apc mutation, resulting in significantly decreased survival and higher intestinal tumor incidence. Accordingly, human CRC cells showed increased tumorigenic properties upon USP22 reduction in vitro and in vivo and induced gene expression signatures associated with an unfavorable outcome in CRC patients. Notably, USP22 loss resulted in increased mTOR activity with the tumorigenic properties elicited by the loss of USP22 being reversible by mTOR inhibitor treatment in vitro and in vivo. Here, we demonstrate that USP22 can exert tumor-suppressive functions in CRC where its loss increases CRC burden by modulating mTOR activity. Importantly, our data uncover a tumor- and context-specific role of USP22, suggesting that USP22 expression could serve as a marker for therapeutic stratification of cancer patients.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.