ArticleCancer letters2019
Downregulation of Epidermal Growth Factor Receptor in hepatocellular carcinoma facilitates Transforming Growth Factor-β-induced epithelial to amoeboid transition.
Article in Cancer letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Uncovering the signaling networks of disseminated glioblastoma cells in vivo with INSIGHT.Nature communications · 2026Article
- Pan-cancer analysis reveals Rho kinase addiction as a vulnerability of de-differentiated cancer cells.iScience · 2026Article
- Amoeboid cancer cells at a glance.Journal of cell science · 2026Review
- Circulating tumor cell-derived lines exhibit an amoeboid mode of migration.Scientific reports · 2026Article
- Targeting CDC42 Protects Mitochondrial Function through KLF2/HIF-1α/PINK1 Signaling in Acute Kidney Injury.International journal of biological sciences · 2026Article
- MiR-423-5p is a metabolic and growth tuner in hepatocellular carcinoma via MALAT-1 and mitochondrial interaction.Journal of experimental & clinical cancer research : CR · 2025Article
- Computational Network Pharmacology, Molecular Docking, and Molecular Dynamics to Decipher Natural Compounds ofPharmaceuticals (Basel, Switzerland) · 2025Article
- NUCKS1 exacerbates hepatocellular carcinoma cell proliferation and metastasis via the upregulation of Cdc42.American journal of cancer research · 2025Article
- The Potential Utility of Circulating Oncofetal H19 Derived miR-675 Expression versus Tissue lncRNA-H19 Expression in Diagnosis and Prognosis of HCC in Egyptian Patients.Biomolecules · 2022Article
- Unravelling cell migration: defining movement from the cell surface.Cell adhesion & migration · 2022Review
- RHO GTPase family in hepatocellular carcinoma.Experimental hematology & oncology · 2022Review
- Amoeboid migration in health and disease: Immune responsesFrontiers in cell and developmental biology · 2022Review
- Role of RhoC in cancer cell migration.Cancer cell international · 2021Review
- Epithelial-Mesenchymal Transition (EMT) Induced by TGF-β in Hepatocellular Carcinoma Cells Reprograms Lipid Metabolism.International journal of molecular sciences · 2021Article
- TGF-β isoforms inhibit hepatitis C virus propagation in transforming growth factor beta/SMAD protein signalling pathway dependent and independent manners.Journal of cellular and molecular medicine · 2021Article
- Phenotypic Plasticity of Cancer Cells Based on Remodeling of the Actin Cytoskeleton and Adhesive Structures.International journal of molecular sciences · 2021Review
- FAM188B Downregulation Sensitizes Lung Cancer Cells to Anoikis via EGFR Downregulation and Inhibits Tumor Metastasis In Vivo.Cancers · 2021Article
- Quantitative Expression of Key Cancer Markers in the AS-30D Hepatocarcinoma Model.Frontiers in oncology · 2021Article
- Review
- Cell Derived Matrix Fibulin-1 Associates With Epidermal Growth Factor Receptor to Inhibit Its Activation, Localization and Function in Lung Cancer Calu-1 Cells.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
The Epidermal Growth Factor Receptor (EGFR) and the Transforming Growth Factor-beta (TGF-β) are key regulators of hepatocarcinogenesis. Targeting EGFR was proposed as a promising therapy; however, poor success was obtained in human hepatocellular carcinoma (HCC) clinical trials. Here, we describe how EGFR is frequently downregulated in HCC patients while TGF-β is upregulated. Using 2D/3D cellular models, we show that after EGFR loss, TGF-β is more efficient in its pro-migratory and invasive effects, inducing epithelial to amoeboid transition. EGFR knock-down promotes loss of cell-cell and cell-to-matrix adhesion, favouring TGF-β-induced actomyosin contractility and acquisition of an amoeboid migratory phenotype. Moreover, TGF-β upregulates RHOC and CDC42 after EGFR silencing, promoting Myosin II in amoeboid cells. Importantly, low EGFR combined with high TGFB1 or RHOC/CDC42 levels confer poor patient prognosis. In conclusion, this work reveals a new tumour suppressor function for EGFR counteracting TGF-β-mediated epithelial to amoeboid transitions in HCC, supporting a rational for targeting the TGF-β pathway in patients with low EGFR expression. Our work also highlights the relevance of epithelial to amoeboid transition in human tumours and the need to better target this process in the clinic.
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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 OpenQuestion graph.