ArticleOncotarget2017
USP22 knockdown enhanced chemosensitivity of hepatocellular carcinoma cells to 5-Fu by up-regulation of Smad4 and suppression of Akt.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- LncRNA TAF1A-AS1 regulates the progression in hepatocellular carcinoma by targeting miR-664b-3p/USP22 axis.Discover oncology · 2026Article
- USP22 regulates APL differentiation via PML-RARα stabilization and IFN repression.Cell death discovery · 2024Article
- Phytochemicals as Potential Lead Molecules against Hepatocellular Carcinoma.Current medicinal chemistry · 2024Review
- Ubiquitin-proteasome pathway-mediated regulation of the Bcl-2 family: effects and therapeutic approaches.Haematologica · 2024Review
- Protein degradation: expanding the toolbox to restrain cancer drug resistance.Journal of hematology & oncology · 2023Review
- Epigenetic remodelling in human hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2022Review
- Article
- Research Progress of DUB Enzyme in Hepatocellular Carcinoma.Frontiers in oncology · 2022Review
- Immune Evasion and Drug Resistance Mediated by USP22 in Cancer: Novel Targets and Mechanisms.Frontiers in immunology · 2022Review
- USP22 promotes HER2-driven mammary carcinoma aggressiveness by suppressing the unfolded protein response.Oncogene · 2021Article
- Molecular Mechanisms of DUBs Regulation in Signaling and Disease.International journal of molecular sciences · 2021Review
- The multiple roles of deubiquitinases in liver cancer.American journal of cancer research · 2020Review
- Inhibition of protein FAK enhances 5-FU chemosensitivity to gastric carcinomaComputational and structural biotechnology journal · 2020Article
- Ubiquitin-specific protease 22 is critical to in vivo angiogenesis, growth and metastasis of non-small cell lung cancer.Cell communication and signaling : CCS · 2019Article
- The role of ubiquitin-specific peptidases in cancer progression.Journal of biomedical science · 2019Review
- TGFβ-Activated USP27X Deubiquitinase Regulates Cell Migration and Chemoresistance via Stabilization of Snail1.Cancer research · 2019Article
- The lncKLF6/KLF6 feedback loop regulates the growth of non-small cell lung cancer.American journal of cancer research · 2018Article
- High expression of USP22 predicts poor prognosis and advanced clinicopathological features in solid tumors: a meta-analysis.OncoTargets and therapy · 2018Article
- Amyloid precursor protein regulates 5-fluorouracil resistance in human hepatocellular carcinoma cells by inhibiting the mitochondrial apoptotic pathway.Journal of Zhejiang University. Science. BArticle
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
USP22, a member of the deubiquitinases (DUBs) family, is known to be a key subunit of the human Spt-Ada-Gcn5 acetyltransferase (hSAGA) transcriptional cofactor complex. Within hSAGA, USP22 removes ubiquitin from histone proteins, thus regulating the transcription and expression of downstream genes. USP22 plays important roles in many cancers; however, its effect and the mechanism underlying HCC chemoresistance remain unclear. In the present study, we found that USP22 was highly expressed in chemoresistant HCC tissues and cells and was correlated with the prognosis of HCC patients who received chemotherapy. Silencing USP22 in chemoresistant HCC Bel/Fu cells dramatically inhibited proliferation, migration, invasion and epithelial-mesenchymal transition in vitro; suppressed tumorigenic and metastatic capacities in vivo; and inhibited drug resistance-related proteins (MDR1, LRP, MRP1). Mechanistically, we found that USP22 knockdown exerts its function through down-regulating PI3K and activating Smad4, which inhibited phosphorylation of Akt. Silencing Smad4 blocked USP22 knockdown-induced Akt inhibition in Bel/Fu cells. Our results, for the first time, provide evidence that USP22 plays a critical role in the development of chemoresistant HCC cells and that high USP22 expression serves as a molecular marker for the prognosis of HCC patients who undergo chemotherapy.
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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.