ArticleOncology letters2021
USP22 promotes melanoma and BRAF inhibitor resistance via YAP stabilization.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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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
8 citing papers in PubMed, 15 citations in OpenAlex.
- Identification of β-Lapachone as a Potent USP22 Inhibitor That Suppresses Cancer Stemness and Enhances Chemosensitivity in Lung Adenocarcinoma.International journal of molecular sciences · 2026Article
- Enhancing cell subpopulation discovery in cancer by integrating single-cell transcriptome and expressed variants.Fundamental research · 2026Article
- Article
- Pitavastatin sensitizes the EGFR-TKI associated resistance in lung cancer by inhibiting YAP/AKT/BAD-BCL-2 pathway.Cancer cell international · 2024Article
- ATXN3 promotes prostate cancer progression by stabilizing YAP.Cell communication and signaling : CCS · 2023Article
- Protein degradation: expanding the toolbox to restrain cancer drug resistance.Journal of hematology & oncology · 2023Review
- RNAi-Based Screening for the Identification of Specific Substrate-Deubiquitinase Pairs.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Review
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Yes-associated protein (YAP) is a conserved transcriptional coactivator that plays key roles in controlling organ size, tumorigenesis and drug resistance. Emerging evidence shows that YAP is overexpressed and associated with resistance to BRAF inhibitor treatment in melanoma. However, the mechanism accounting for YAP-overexpression in melanoma is largely unknown. The present study characterized ubiquitin-specific peptidase 22 (USP22) as a deubiquitinase controlling YAP abundance and biological functions in melanoma. Using western blotting and immunohistochemical staining, it was found that the expression of USP22 and YAP was associated in melanoma cell lines and patient samples. Moreover, USP22 interacted with and deubiquitinated YAP to prevent YAP turnover. Depletion of USP22 decreased YAP expression, which in turn suppressed cell proliferation and tumorigenesis. Furthermore, overexpression of USP22 conferred vemurafenib resistance in a YAP-dependent manner. Overall, the present study revealed the important role of the USP22/YAP axis in melanoma and BRAF inhibitor resistance, and provides a rationale to target USP22/YAP for melanoma treatment.
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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 Socratic graph.