ArticleInternational journal of molecular sciences2014
USP22 promotes NSCLC tumorigenesis via MDMX up-regulation and subsequent p53 inhibition.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- Overexpression and Biological Function of Ubiquitin-Specific Protease 42 in Gastric Cancer.PloS one · 2016Trial
- The deubiquitinating enzyme USP42 promotes lung adenocarcinoma progression through PTGS2.Journal of molecular histology · 2026Article
- Roles of ubiquitin‑specific peptidase 22 in cellular fate: From embryonic survival to tissue repair, inflammation and metabolism (Review).International journal of molecular medicine · 2026Review
- Targeting ubiquitin-specific peptidase 22 in solid tumours: from ubiquitination to immunotherapy.Frontiers in cell and developmental biology · 2026Review
- USP22 promotes gefitinib resistance and inhibits ferroptosis in non-small cell lung cancer by deubiquitination of MDM2.Thoracic cancer · 2024Article
- Friend or foe? Reciprocal regulation between E3 ubiquitin ligases and deubiquitinases.Biochemical Society transactions · 2024Review
- Silencing of mAmerican journal of cancer research · 2023Article
- Targeted therapy based on ubiquitin-specific proteases, signalling pathways and E3 ligases in non-small-cell lung cancer.Frontiers in oncology · 2023Review
- Immune Evasion and Drug Resistance Mediated by USP22 in Cancer: Novel Targets and Mechanisms.Frontiers in immunology · 2022Review
- Article
- Biological effects of ubiquitin-specific peptidase 22 on thyroid papillary cancer cells and its mechanism of action.Translational cancer research · 2020Article
- USP22 promotes development of lung adenocarcinoma through ubiquitination and immunosuppression.Aging · 2020Article
- USP22 exerts tumor-suppressive functions in colorectal cancer by decreasing mTOR activity.Cell death and differentiation · 2020Article
- Article
- USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta.Development (Cambridge, England) · 2019Article
- Control of CCND1 ubiquitylation by the catalytic SAGA subunit USP22 is essential for cell cycle progression through G1 in cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- The ASH1-miR-375-YWHAZ Signaling Axis Regulates Tumor Properties in Hepatocellular Carcinoma.Molecular therapy. Nucleic acids · 2018Article
- Downregulation of Ubiquitin-Specific Protease 22 Inhibits Proliferation, Invasion, and Epithelial-Mesenchymal Transition in Osteosarcoma Cells.Oncology research · 2017Article
- The Emerging Role of Non-traditional Ubiquitination in Oncogenic Pathways.The Journal of biological chemistry · 2017Review
- Prognostic and clinicopathological significance of ubiquitin-specific protease 22 overexpression in cancers: evidence from a meta-analysis.OncoTargets and therapy · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence suggests that ubiquitin-specific protease 22 (USP22) has great clinicopathologic significance in oncology. In this study, we investigated the role of USP22 in human NSCLC tumorigenesis along with the underlying mechanisms of action. First, we determined the expression of USP22 in human NSCLC, as well as normal tissues and cell lines. We then studied the effects of USP22 silencing by shRNA on NSCLC cell growth in vitro and tumorigenesis in vivo, along with the effect on the p53 pathway. We found that USP22 is overexpressed in human NSCLC tissues and cell lines. USP22 silencing by shRNA inhibits proliferation, induces apoptosis and arrests cells at the G0/G1 phases in NSCLC cells and curbs human NSCLC tumor growth in a mouse xenograft model. Additionally, USP22 silencing downregulates MDMX protein expression and activates the p53 pathway. Our co-immunoprecipitation analysis shows that USP22 interacts with MDMX in NSCLC cells. Furthermore, MDMX silencing leads to growth arrest and apoptosis in NSCLC cells, and over-expression of MDMX reverses the USP22 silencing-induced effects. Taken together, our results suggest that USP22 promotes NSCLC tumorigenesis in vitro and in vivo through MDMX upregulation and subsequent p53 inhibition. USP22 may represent a novel target for NSCLC treatment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.