ArticleCancer cell international2017
Dual EGFR and BRAF blockade overcomes resistance to vemurafenib in BRAF mutated thyroid carcinoma cells.
Article in Cancer cell international, 2017. 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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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Design and synthesis of novel thiazole/1,2,4-triazole/quinoline hybrids as antiproliferative agents, apoptosis inducers, immunomodulators, and multi-EGFR/BRAFMolecular diversity · 2026Article
- In-silico studies, synthesis, and pharmacological screening of novel multitarget diphenylpyrazole scaffold as EGFR/BRAF and cyclooxygenase-2 inhibitors.Scientific reports · 2025Article
- Design, synthesis, and antiproliferative activity of new 1,2,3-triazole/quinazoline-4-one hybrids as dual EGFR/BRAFRSC advances · 2024Article
- Design and synthesis of new 1,2,4-oxadiazole/quinazoline-4-one hybrids with antiproliferative activity as multitargeted inhibitors.Frontiers in chemistry · 2024Article
- New 1,2,3-triazole/1,2,4-triazole hybrids linked to oxime moiety as nitric oxide donor selective COX-2, aromatase, B-RAFJournal of enzyme inhibition and medicinal chemistry · 2023Article
- Design, Synthesis, and Biological Evaluation of Novel 3-Cyanopyridone/Pyrazoline Hybrids as Potential Apoptotic Antiproliferative Agents Targeting EGFR/BRAFMolecules (Basel, Switzerland) · 2023Article
- Design, Synthesis, Antiproliferative Actions, and DFT Studies of New Bis-Pyrazoline Derivatives as Dual EGFR/BRAFInternational journal of molecular sciences · 2023Article
- One-Pot Synthesis of 1-Thia-4-azaspiro[4.4/5]alkan-3-ones via Schiff Base: Design, Synthesis, and Apoptotic Antiproliferative Properties of Dual EGFR/BRAFPharmaceuticals (Basel, Switzerland) · 2023Article
- Role of IL-6/STAT3 Axis in Resistance to Cisplatin in Gastric Cancers.Biomedicines · 2023Article
- Review
- Papillary thyroid cancer organoids harboring BRAFJournal of translational medicine · 2023Article
- The AhR-SRC axis as a therapeutic vulnerability in BRAFi-resistant melanoma.EMBO molecular medicine · 2022Article
- Regulated cell death (RCD) in cancer: key pathways and targeted therapies.Signal transduction and targeted therapy · 2022Review
- BRAF Inhibitors Induce Feedback Activation of RAS Pathway in Thyroid Cancer Cells.International journal of molecular sciences · 2021Article
- Targeted Therapy of Papillary Thyroid Cancer: A Comprehensive Genomic Analysis.Frontiers in endocrinology · 2021Article
- Review
- Combinatorial Therapies in Thyroid Cancer: An Overview of Preclinical and Clinical Progresses.Cells · 2020Review
- VCAM-1 Upregulation Contributes to Insensitivity of Vemurafenib in BRAF-Mutant Thyroid Cancer.Translational oncology · 2020Article
- BRAF Inhibitors in Thyroid Cancer: Clinical Impact, Mechanisms of Resistance and Future Perspectives.Cancers · 2019Review
- Preclinical Evaluation of Vemurafenib as Therapy for BRAFInternational journal of molecular sciences · 2018Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBRAF inhibitors are effective anticancer agents in BRAF-mutated melanomas. By contrast, evidences about sensitivity of thyroid carcinomas to BRAF inhibition are conflicting and it has been proposed that BRAF V600E thyroid carcinoma cells are less sensitive to BRAF inhibitors due to activation of parallel signaling pathways. This study evaluated the hypothesis that feedback activation of EGFR signaling counteracts the cytostatic activity of vemurafenib (PLX4032) in BRAF V600E thyroid carcinoma cells.
methodsCell proliferation, cell cycle distribution, induction of apoptosis and EGFR and AKT signaling were evaluated in thyroid carcinoma cell lines bearing the BRAF V600E mutation in response to PLX4032.
resultsA partial and transient cytostatic response to PLX4032 was observed in thyroid carcinoma cell lines bearing the BRAF V600E mutation, with lack of full inhibition of ERK pathway. Interestingly, the exposure of thyroid carcinoma cells to PLX4032 resulted in a rapid feedback activation of EGFR signaling with parallel activation of AKT phosphorylation. Consistently, the dual inhibition of EGFR and BRAF, through combination therapy with PLX4032 and gefitinib, resulted in prevention of EGFR phosphorylation and sustained inhibition of ERK and AKT signaling and cell proliferation. Of note, the combined treatment with gefitinib and vemurafenib or the exposure of EGFR-silenced thyroid carcinoma cells to vemurafenib induced synthetic lethality compared to single agents.
conclusionsThese data suggest that the dual EGFR and BRAF blockade represents a strategy to by-pass resistance to BRAF inhibitors in thyroid carcinoma cells.
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