ArticleCellular oncology (Dordrecht, Netherlands)2023
USP13 promotes breast cancer metastasis through FBXL14-induced Twist1 ubiquitination.
Article in Cellular oncology (Dordrecht, Netherlands), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Role of epithelial-mesenchymal transition (EMT) in malignancies: current status and future prospects.Signal transduction and targeted therapy · 2026Review
- Dynamic feedback between IL-6 and TWIST1 drives pancreatic cancer progression.Translational gastroenterology and hepatology · 2026Article
- Hypoxia-induced USP13 expression drives ferroptosis resistance and tumor immune evasion in hepatocellular carcinoma through the stabilization of ACLY.Cell death discovery · 2025Article
- Ubiquitin-specific protease 13 promotes colorectal cancer progression by stabilizing mitogen-activated protein kinase kinase 3.Molecular biomedicine · 2025Article
- Non-classic deubiquitinase USP13 inhibits bladder cancer metastasis through destabilizing cytoplasmic KDM3A.Oncogene · 2025Article
- YY1 induced USP13 transcriptional activation drives the malignant progression of hepatocellular carcinoma by deubiquitinating WWP1.Cellular & molecular biology letters · 2025Article
- Bruceine A Inhibits Cell Proliferation by Targeting the USP13/PARP1 Signalling Pathway in Multiple Myeloma.Basic & clinical pharmacology & toxicology · 2025Article
- Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025Review
- Exploring Autophagy-Related Gene Expression in Hepatocellular Carcinoma via TCGA, GEPIA2, and HPA Databases: Implications for Prognosis.Journal of hepatocellular carcinoma · 2025Article
- F-box in breast cancer: mechanism of action and therapeutic potential.American journal of translational research · 2025Review
- Modulation of Epithelial-Mesenchymal Transition Is a Possible Underlying Mechanism for Inducing Chemoresistance in MIA PaCa-2 Cells against Gemcitabine and Paclitaxel.Biomedicines · 2024Article
- Roles of ubiquitin‑specific protease 13 in normal physiology and tumors (Review).Oncology letters · 2024Review
- δ-catenin promotes Twist1 stabilization in prostate cancer through ubiquitination modification.American journal of cancer research · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeEpithelial-to-mesenchymal transition (EMT) is an important cause of high mortality in breast cancer. Twist1 is one of the EMT transcription factors (EMT-TFs) with a noticeably short half-life, which is regulated by proteasome degradation pathways. Recent studies have found that USP13 stabilizes several specific oncogenic proteins. As yet, however, the relationship between Twist1 and USP13 has not been investigated.
methodsCo-Immunoprecipitation, GST-pulldown, Western blot, qRT-PCR and immunofluorescence assays were used to investigate the role of USP13 in de-ubiquitination of Twist1. Chromatin immunoprecipitation and Luciferase reporter assays were used to investigate the role of Twist1 in inhibiting USP13 reporter transcription. Scratch wound healing, cell migration and invasion assays, and a mouse lung metastases assay were used to investigate the roles of USP13 and Twist1 in promoting breast cancer metastasis.
resultsWe found that Twist1 can be de-ubiquitinated by USP13. In addition, we found that the protein levels of Twist1 dose-dependently increased with USP13 overexpression, while USP13 knockdown resulted in a decreased expression of endogenous Twist1. We also found that USP13 can directly interact with Twist1 and specifically cleave the K48-linked polyubiquitin chains of Twist1 induced by FBXL14. We found that the effect of USP13 in promoting the migration and invasion capacities of breast cancer cells can at least partly be achieved through its regulation of Twist1, while Twist1 can inhibit the transcriptional activity of USP13.
conclusionsOur data indicate that an interplay between Twist1 and USP13 can form a negative physiological feedback loop. Our findings show that USP13 may play an essential role in breast cancer metastasis by regulating Twist1 and, as such, provide a potential target for the clinical treatment of breast cancer.
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