ArticleNature communications2020
A self-sustaining endocytic-based loop promotes breast cancer plasticity leading to aggressiveness and pro-metastatic behavior.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Mechanisms of active wetting and fluidification in epithelial cell collectives.Nature materials · 2026Article
- G4mer: An RNA language model for transcriptome-wide identification of G-quadruplexes and disease variants from population-scale genetic data.Nature communications · 2025Article
- Epsin3 promotes non-small cell lung cancer progression via modulating EGFR stability.Cell & bioscience · 2025Article
- Comprehensive analytical approach identifies a subtype of CTCF+ tumor-associated neutrophils associated with CRC development and as a biomarker for immunotherapy.International journal of biological sciences · 2025Article
- TBC1 domain-containing proteins are frequently involved in triple-negative breast cancers in connection with the induction of a glycolytic phenotype.Cell death & disease · 2024Article
- Lowering expression of Epsin-3 inhibits migration and invasion of lung adenocarcinoma cells by inhibiting the epithelial-mesenchymal transition.Scientific reports · 2024Article
- A PET-Surrogate Signature for the Interrogation of the Metabolic Status of Breast Cancers.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- MIF is a critical regulator of mononuclear phagocytic infiltration in hepatocellular carcinoma.iScience · 2023Article
- Endocytosis in cancer and cancer therapy.Nature reviews. Cancer · 2023Review
- Interferon-alpha responsible EPN3 regulates hepatitis B virus replication.Frontiers in medicine · 2022Article
- Mesenchymal Stem Cells and their Derived Exosomes Promote Malignant Phenotype of Polyploid Non-Small-Cell Lung Cancer Cells through AMPK Signaling Pathway.Analytical cellular pathology (Amsterdam) · 2022Article
- The role of microfibrillar-associated protein 2 in cancer.Frontiers in oncology · 2022Review
- Epsin 3 potentiates the NF‑κB signaling pathway to regulate apoptosis in breast cancer.Molecular medicine reports · 2022Article
- Endocytosis in the context-dependent regulation of individual and collective cell properties.Nature reviews. Molecular cell biology · 2021Review
- Using dynamic cell communication improves treatment strategies of breast cancer.Cancer cell international · 2021Review
- Autocrine TGF-β in Cancer: Review of the Literature and Caveats in Experimental Analysis.International journal of molecular sciences · 2021Review
- A Four-Gene-Based Prognostic Model Predicts Overall Survival in Patients With Cutaneous Melanoma.Frontiers in oncology · 2021Article
- The Potential Prognostic Role of Oligosaccharide-Binding Fold-Containing Protein 2A (OBFC2A) in Triple-Negative Breast Cancer.Frontiers in oncology · 2021Article
Corrections and comments
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Authors and funding
22 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The subversion of endocytic routes leads to malignant transformation and has been implicated in human cancers. However, there is scarce evidence for genetic alterations of endocytic proteins as causative in high incidence human cancers. Here, we report that Epsin 3 (EPN3) is an oncogene with prognostic and therapeutic relevance in breast cancer. Mechanistically, EPN3 drives breast tumorigenesis by increasing E-cadherin endocytosis, followed by the activation of a β-catenin/TCF4-dependent partial epithelial-to-mesenchymal transition (EMT), followed by the establishment of a TGFβ-dependent autocrine loop that sustains EMT. EPN3-induced partial EMT is instrumental for the transition from in situ to invasive breast carcinoma, and, accordingly, high EPN3 levels are detected at the invasive front of human breast cancers and independently predict metastatic rather than loco-regional recurrence. Thus, we uncover an endocytic-based mechanism able to generate TGFβ-dependent regulatory loops conferring cellular plasticity and invasive behavior.
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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.