ArticleTargeted oncology2015
Expression and activity of EGFR in human cutaneous melanoma cell lines and influence of vemurafenib on the EGFR pathway.
Article in Targeted oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 43 citations in OpenAlex.
- PTRF Confers Melanoma-Acquired Drug Resistance Through the Upregulation of EGFR.Cell proliferation · 2026Article
- Recombinant Oncolytic Vesicular Stomatitis Virus Expressing Mouse Interleukin-12 and Granulocyte-Macrophage Colony-Stimulating Factor (rVSV-dM51-mIL12-mGMCSF) for Immunotherapy of Lung Carcinoma.International journal of molecular sciences · 2025Article
- Global trends and emerging insights in BRAF and MEK inhibitor resistance in melanoma: a bibliometric analysis.Frontiers in molecular biosciences · 2025Article
- Characterization of two melanoma cell lines resistant to BRAF/MEK inhibitors (vemurafenib and cobimetinib).Cell communication and signaling : CCS · 2024Article
- Development of trisubstituted thiophene-3-arboxamide selenide derivatives as novel EGFR kinase inhibitors with cytotoxic activity.RSC medicinal chemistry · 2023Article
- Anticancer Effect of Cold Atmospheric Plasma in Syngeneic Mouse Models of Melanoma and Colon Cancer.Molecules (Basel, Switzerland) · 2023Article
- The AhR-SRC axis as a therapeutic vulnerability in BRAFi-resistant melanoma.EMBO molecular medicine · 2022Article
- Aloysia Citrodora Essential Oil Inhibits Melanoma Cell Growth and Migration by Targeting HB-EGF-EGFR Signaling.International journal of molecular sciences · 2021Article
- The Role of Senescent Cells in Acquired Drug Resistance and Secondary Cancer in BRAFi-Treated Melanoma.Cancers · 2021Review
- Ferroptosis-Associated Classifier and Indicator for Prognostic Prediction in Cutaneous Melanoma.Journal of oncology · 2021Review
- Review
- Melittin fromAntibiotics (Basel, Switzerland) · 2020Article
- Targeted Therapy in Melanoma and Mechanisms of Resistance.International journal of molecular sciences · 2020Review
- Article
- Combination of Selected MET and EGFR Inhibitors Decreases Melanoma Cells' Invasive Abilities.Frontiers in pharmacology · 2019Article
- Wild-type KRAS is a novel therapeutic target for melanoma contributing to primary and acquired resistance to BRAF inhibition.Oncogene · 2018Article
- Potential therapeutic targets of epithelial-mesenchymal transition in melanoma.Cancer letters · 2017Review
- Oncodomains: A protein domain-centric framework for analyzing rare variants in tumor samples.PLoS computational biology · 2017Article
- Antiangiogenic antibody improves melanoma detection by fluorescently labeled therapeutic antibodies.The Laryngoscope · 2016Article
- Efficacy of BRAF Inhibitors in Asian Metastatic Melanoma Patients: Potential Implications of Genomic Sequencing in BRAF-Mutated Melanoma.Translational oncology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Data regarding the expression of epidermal growth factor receptor (EGFR) in melanoma and its role in the tumor biology are conflicting. In BRAF V600-mutant melanomas, the expression of EGFR has been associated with acquired resistance to BRAF inhibitors. In this study, we assessed EGFR expression and downstream signaling activity in a panel of melanoma cell lines and we investigated the effects of the BRAF inhibitor vemurafenib on expression of EGFR and its downstream effectors in a subgroup of BRAF-mutant melanoma cells. Three out of 10 melanoma cell lines expressed EGFR. Downstream signaling via ERK and AKT was responsive to either stimulation by EGF or inhibition by erlotinib. Constitutive activation of ERK occurred in all the cell lines investigated whereas constitutive activation of AKT only in three cell lines. Constitutive activation of ERK and AKT was independent from EGFR expression. Vemurafenib did not affect EGFR expression in general, but it increased EGFR phosphorylation in the cell line SkMel5. Induced EGFR phosphorylation was sensitive to treatment with erlotinib. Vemurafenib efficiently blocked ERK activation in all the BRAF-mutant cell lines tested, whereas its effects on AKT activation were dissimilar in the different cell lines. Our data suggest that EGFR is functional but usually inactive in EGFR high-expressing cell lines. Basal EGFR expression unlikely represents a biomarker for predicting the sensitivity to vemurafenib in melanoma, but EGFR activation might represent a mechanism of vemurafenib resistance in a subset of melanoma cells.
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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.