ArticleOncology research2016
Suppression of Ubiquitin-Specific Peptidase 17 (USP17) Inhibits Tumorigenesis and Invasion in Non-Small Cell Lung Cancer Cells.
Article in Oncology research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Assessment of USP17 and TPT1 Expression in Primary and Matched Metastatic Tissue of Patients with High-Grade Serous Ovarian Carcinoma and the Relationship to Distant Metastasis.Diagnostics (Basel, Switzerland) · 2026Article
- The deubiquitinase USP17 regulates the expression and activity of the oncogenic driver β-catenin in colorectal cancer.Oncogene · 2026Article
- Ubiquitination and deubiquitination as critical modulators of NSCLC tumorigenesis and drug resistance.Discover oncology · 2026Review
- C4orf19 inhibits colorectal cancer cell proliferation by competitively binding to Keap1 with TRIM25 via the USP17/Elk-1/CDK6 axis.Oncogene · 2023Article
- Ubiquitin-specific protease 3 facilitates cell proliferation by deubiquitinating pyruvate kinase L/R in gallbladder cancer.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- The emerging role of ubiquitin-specific protease 20 in tumorigenesis and cancer therapeutics.Cell death & disease · 2022Review
- USP17 is required for peripheral trafficking of lysosomes.EMBO reports · 2022Article
- The role of the deubiquitinating enzyme DUB3/USP17 in cancer: a narrative review.Cancer cell international · 2021Review
- Deubiquitinating enzyme USP41 promotes lung cancer cell proliferation and migration.Thoracic cancer · 2021Article
- Advances in deubiquitinating enzymes in lung adenocarcinoma.Journal of Cancer · 2021Review
- Ubiquitin-specific peptidase 17 promotes cisplatin resistance via PI3K/AKT activation in non-small cell lung cancer.Oncology letters · 2020Article
- The ubiquitin system: orchestrating cellular signals in non-small-cell lung cancer.Cellular & molecular biology letters · 2020Review
- DUB3 Facilitates Growth and Inhibits Apoptosis Through Enhancing Expression of EZH2 in Oral Squamous Cell Carcinoma.OncoTargets and therapy · 2020Article
- Simulated microgravity with floating environment promotes migration of non-small cell lung cancers.Scientific reports · 2019Article
- The miR-195 Axis Regulates Chemoresistance through TUBB and Lung Cancer Progression through BIRC5.Molecular therapy oncolytics · 2019Article
- Ubiquitin-Proteasome Axis, Especially Ubiquitin-Specific Protease-17 (Reproductive sciences (Thousand Oaks, Calif.) · 2019Article
- Article
- An age-based, RNA expression paradigm for survival biomarker identification for pediatric neuroblastoma and acute lymphoblastic leukemia.Cancer cell international · 2019Article
- USP17 mediates macrophage-promoted inflammation and stemness in lung cancer cells by regulating TRAF2/TRAF3 complex formation.Oncogene · 2018Article
- USP17 is required for trafficking and oncogenic signaling of mutant EGFR in NSCLC cells.Cell communication and signaling : CCS · 2018Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, deubiquitinating enzymes (DUBs) are emerging as new regulators in cancer progression. However, understanding of the involvement of DUBs in non-small cell lung cancer (NSCLC) is just beginning. In this study, we investigated the expression and biological function of ubiquitin-specific peptidase 17 (USP17) in NSCLC progression in vitro and in vivo. We found that the expression of USP17 was higher than in a normal control. We further efficiently depleted USP17 expression in two different NSCLC cells, A549 and H1299. The anchorage-independent growth ability of these cells, estimated by soft agar colony formation assay, was significantly reduced after USP17 knockdown. Moreover, Matrigel-Transwell analysis showed that suppression of USP17 decreased cell migration and invasion capacity. Molecular mechanism studies found that USP17 silencing downregulated the expression of matrix metalloproteases (MMP3 and MMP9) in NSCLC cells. Furthermore, animal model results showed that USP17 suppression inhibited NSCLC tumorigenesis and growth. Altogether, this study illustrates the important functions of USP17 in NSCLC and suggests that USP17 might be an attractive target for NSCLC therapy.
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