ArticleBritish journal of cancer2023
Targeting metabolism by B-raf inhibitors and diclofenac restrains the viability of BRAF-mutated thyroid carcinomas with Hif-1α-mediated glycolytic phenotype.
Article in British journal of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 16 citations in OpenAlex.
- [Methyltransferase-like protein 7B promotes glycolysis and malignant progression in papillary thyroid carcinoma cells via the USP28/HIF-1α axis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Article
- Targeting the Warburg Effect in Anaplastic Thyroid Carcinoma: Metabolic Vulnerabilities and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Glucose Metabolic Reprogramming in Thyroid Cancer: Underlying Molecular Mechanisms and Links to Progression and Treatment.Current medical science · 2026Review
- Review
- The Yin-Yang balance of SIRT1 and SIRT2 in cancer metabolic remodeling.International journal of biological sciences · 2026Review
- Thyroid cancer: From molecular insights to therapy (Review).Oncology letters · 2025Review
- Targeting Metabolic Pathways in AML Cell Lines: Impact of Hypoxia-Inducible Factor-1α (HIF-1α) and Lactate Dehydrogenase-A (LDH-A) Inhibition.Iranian biomedical journal · 2025Article
- IL-9 Promotes Migratory Dissemination of Malignant T Cells by Activating the HIF-1α-Cofilin-1 Axis in Cutaneous T-cell Lymphoma.Molecular cancer research : MCR · 2025Article
- Reprogramming of Thyroid Cancer Metabolism: from Mechanism to Therapeutic Strategy.Molecular cancer · 2025Review
- UnravelingCancer drug resistance (Alhambra, Calif.) · 2025Article
- Developments in the study of the role of lactate metabolism in the genesis and progression of thyroid cancer.Frontiers in cell and developmental biology · 2025Review
- A computational approach to assessing the prognostic implications of BRAF and RAS mutations in patients with papillary thyroid carcinoma.Endocrine · 2024Article
- Integrated proteogenomic and metabolomic characterization of papillary thyroid cancer with different recurrence risks.Nature communications · 2024Article
- Targeting Hypoxia-Inducible Factor-1 (HIF-1) in Cancer: Emerging Therapeutic Strategies and Pathway Regulation.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Revolutionizing Cancer Treatment: Unveiling New Frontiers by Targeting the (Un)Usual Suspects.Cancers · 2023Article
- Update on current diagnosis and management of anaplastic thyroid carcinoma.World journal of clinical oncology · 2023Review
- Toward Systems-Level Metabolic Analysis in Endocrine Disorders and Cancer.Endocrinology and metabolism (Seoul, Korea) · 2023Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundB-raf inhibitors (BRAFi) are effective for BRAF-mutated papillary (PTC) and anaplastic (ATC) thyroid carcinomas, although acquired resistance impairs tumour cells' sensitivity and/or limits drug efficacy. Targeting metabolic vulnerabilities is emerging as powerful approach in cancer.
methodsIn silico analyses identified metabolic gene signatures and Hif-1α as glycolysis regulator in PTC. BRAF-mutated PTC, ATC and control thyroid cell lines were exposed to HIF1A siRNAs or chemical/drug treatments (CoCl
resultsA specific metabolic gene signature was identified as a hallmark of BRAF-mutated tumours, which display a glycolytic phenotype, characterised by enhanced glucose uptake, lactate efflux and increased expression of Hif-1α-modulated glycolytic genes. Indeed, Hif-1α stabilisation counteracts the inhibitory effects of BRAFi on these genes and on cell viability. Interestingly, targeting metabolic routes with BRAFi and diclofenac combination we could restrain the glycolytic phenotype and synergistically reduce tumour cells' viability.
conclusionThe identification of a metabolic vulnerability of BRAF-mutated carcinomas and the capacity BRAFi and diclofenac combination to target metabolism open new therapeutic perspectives in maximising drug efficacy and reducing the onset of secondary resistance and drug-related toxicity.
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