ArticleCancer medicine2024
Fibroblast Growth Factor Receptor 4 Promotes Triple-Negative Breast Cancer Progression via Regulating Fatty Acid Metabolism Through the AKT/RYR2 Signaling.
Article in Cancer medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Investigation of Fatty Acid Metabolism-Associated Molecular CPOX and the Underlying Mechanism in Follicular Lymphoma.Biochemical genetics · 2026Article
- Prognostic and clinicopathologic significance of FGFR mRNA and protein overexpression in colorectal cancer: a systematic review and meta-analysis.Translational cancer research · 2026Article
- ANXA1-Derived Peptide Increases Melanoma Cell Sensitivity to Vemurafenib by Downregulating EphA2.Journal of cellular and molecular medicine · 2026Article
- Targeted antibody-drug conjugates for rhabdomyosarcoma and other FGFR4-expressing cancers.Cell reports. Medicine · 2026Article
- Multi-omic Profiling of Recurrence Risk Across Breast Cancer Subtypes.medRxiv : the preprint server for health sciences · 2026Article
- Identification of a prognostic model using immune related genes combined with tumour mutational burden and T cell infiltration in triple-negative breast cancer.Oncology letters · 2026Article
- Targeting RSK2 enhances the efficacy of IGF1R inhibitor against triple-negative breast cancer via antagonizing IGF1/IGF1R signaling mediated by GATA3-IGFBP5 pathway.Acta pharmacologica Sinica · 2026Article
- Multi-Omics and Machine Learning-Uncovered FLT1-Mediated Epithelial-Endothelial Crosstalk in Cellular Senescence Driving Clear Cell Renal Cell Carcinoma Malignancy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- ATP2C2-PLA2R1 axis underlies lipid metabolism modulation and invasion in papillary thyroid carcinoma mediated by a VGIC signature.Discover oncology · 2026Article
- Isoliquiritigenin Suppresses Oral Squamous Cell Carcinoma Progression by Targeting FABP5-Mediated Lipid Metabolism: Association with the circPOLB/miR-548ae-3p/C-MYC Axis.Oncology research · 2026Article
- ELOVL6 Promotes the Proliferation and Migration of Oral Squamous Cell Carcinoma Cells Through Fatty Acid Remodelling and ROS Modulation in vitro.OncoTargets and therapy · 2026Article
- Evaluating the potential causal relationship between carnitine-related metabolites and breast cancer: a Mendelian randomization and transcriptomic analysis.Archives of medical science : AMS · 2026Article
- CES3 promotes NSCLC progression via lipid metabolic reprogramming regulated by TFAP2A.Journal of Cancer · 2026Article
- The role of fibroblast growth factors in cell and cancer metabolism.FEBS letters · 2026Review
- Breast Cancer Progression by the FGF/FGFR Axis: A Metabolic Perspective.Journal of mammary gland biology and neoplasia · 2025Review
- UPP1/ARNT positive feedback loop drives gastric cancer progression through metabolism reprogramming.Medical oncology (Northwood, London, England) · 2025Article
- Over-Expression of TNFRSF12A Promotes Immune Suppression and Facilitates Angiogenesis in Triple-Negative Breast Cancer.Biology · 2025Article
- FGF4 drives tumor progression in triple-negative breast cancer via IL6/STAT3-mediated macrophage M2 polarization and immune suppression.Cell division · 2025Article
- Mechanistic study on the inhibition of triple-negative breast cancer progression by LncRNA TFAP2A-AS1 through the regulation of miR-6892/PHGDH.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundTriple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer. Previous studies have found that fibroblast growth factor receptor 4 (FGFR4) plays a crucial role in tumor development and metastasis. However, the potential role and underlying mechanisms of FGFR4 in the progression of TNBC remain unclear.
methodsStatistical analysis of FGFR4 expression data in public databases was used to reveal its role in TNBC. qRT-PCR was used to detect FGFR4 expression levels. The impact of FGFR4 level changes on TNBC cell proliferation was assessed using CCK-8 and colony formation assays, while Transwell invasion assays and JC-1 staining were employed to analyze the effects of FGFR4 level changes on the invasiveness and survival capability of TNBC cells. Differentially expressed genes were subjected to Gene Ontology, KEGG, and GSEA enrichment analyses to identify associated signaling pathways. Additionally, Oil Red O staining, fatty acid metabolite detection, and Western blot analysis were used to investigate the impact of FGFR4 and its inhibitor fisogatinib, as well as the AKT activator SC79, on the metabolic reprogramming of fatty acids in TNBC cells.
resultsFGFR4 was found to be upregulated in breast cancer and correlated with poorer patient outcomes. Inhibition of FGFR4 resulted in reduced cell growth and invasion in TNBC cells. It also led to increased lipid accumulation, upregulated lipid biosynthesis-related genes, and downregulated lipolysis-related genes. Mechanistically, FGFR4 inhibition suppressed the activation of the AKT/RYR2 signaling pathway. Reactivating the AKT pathway reversed the suppressive effects of FGFR4 inhibition on TNBC progression.
conclusionDysregulated FGFR4 activates the AKT/RYR2 axis, leading to tumor proliferation, invasion, and altered lipid metabolism in TNBC. FGFR4 inhibition could potentially serve as a novel therapeutic strategy for TNBC treatment.
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