ArticleCellular & molecular biology letters2025
YY1 induced USP13 transcriptional activation drives the malignant progression of hepatocellular carcinoma by deubiquitinating WWP1.
Article in Cellular & molecular biology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- PDIA6 exacerbates hepatocellular carcinoma via enhancing proteasome-dependent degradation of AKAP12.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- A tale of dual role: HECT‑type E3 ubiquitin ligase mechanisms in liver diseases (Review).International journal of molecular medicine · 2026Review
- A positive feedback loop between BACH1 and IL-1β promotes the progression of HPV-negative head and neck squamous cell carcinoma.Cell communication and signaling : CCS · 2026Article
- Mapping Genetic Regulation of Transcription to Identify Functional Variants and Genes Associated with Pancreatic Cancer Risk.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Simultaneous Inhibition of ACLY and OGDH Has a Synergistic Effect on Hepatocellular Carcinoma Cell Lines.bioRxiv : the preprint server for biology · 2026Article
- Targeting the Notch1-YY1-ICAM1 Signaling Axis Enhances the Efficacy of Immunotherapy in HCC by Activating CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- FBXO42 promotes hepatocellular carcinoma progression via mediating p57Kip2 ubiquitination and degradation.European journal of medical research · 2025Article
- UBE2V1 Promotes Hepatocellular Carcinoma Progression by Forming a Positive Feedback Loop with HIF-1α.Research (Washington, D.C.) · 2025Article
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17 authors.
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Abstract
backgroundHepatocellular carcinoma (HCC) is the sixth most prevalent cancer globally and the third leading cause of cancer-related mortality. Protein ubiquitination and deubiquitination play vital roles in human cancers. Ubiquitin-specific protease 13 (USP13) is a deubiquitinating enzyme (DUB) that is involved in many cellular processes. However, the mechanism by which USP13 regulates deubiquitination remains largely unknown.
methodsClinical data were analyzed via online databases. USP13 expression in HCC cell lines and tissues was analyzed via western blotting and immunohistochemistry. A lentivirus was used to established stable USP13-knockdown and USP13-overexpression cells. Cell Counting Kit-8, colony formation, wound healing, Transwell, and sphere formation assays were used to detect the malignant behaviors of HCC cells in vitro. A subcutaneous mouse model was used to investigate the function of USP13 in vivo. Co-immunoprecipitation, chromatin immunoprecipitation and dual-luciferase reporter assays were conducted to explore the molecular regulation.
resultsUSP13 was upregulated in HCC cell lines and tissues, which predicted a poor prognosis in patients with HCC. Functional experiments in which USP13 was overexpressed or depleted revealed the oncogenic role of USP13 in driving HCC progression both in vitro and in vivo. Mechanistically, WW domain-containing ubiquitin E3 ligase 1 (WWP1) was identified as a binding protein of USP13. Furthermore, USP13 can interact with WWP1 and then remove the K29- and K48-linked polyubiquitination chains from WWP1 to stabilize the WWP1 protein via the ubiquitin-proteasome pathway. Moreover, Yin Yang 1 (YY1) was explored as a new transcription factor of USP13, and YY1 could also upregulate WWP1 expression through USP13. Moreover, YY1 and WWP1 were shown to participate in the oncogenic role of USP13.
conclusionsOur findings revealed the functional YY1/USP13/WWP1 signaling axis in HCC, identifying a promising therapeutic target for anti-HCC treatment.
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