ArticleJournal of experimental & clinical cancer research : CR2025
Adipocytes-induced ANGPTL4/KLF4 axis drives glycolysis and metastasis in triple-negative breast cancer.
Article in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Current and Future Perspectives on Adipo-Oncology: Roles of Adipocytes in Local and Systemic Tumor Regulation.Pathology international · 2026Review
- Adipocyte-rich microenvironment promotes TNBC progression through SIRT6-associated ACSL5 dysregulation and lipid storage-associated phenotypes.Journal of experimental & clinical cancer research : CR · 2026Article
- Disruption of YAP biomolecular condensates by mechanical stress drives intervertebral disc vascularization.Science advances · 2026Article
- Proteomic signatures of adipocyte recruitment in breast cancer.Endocrine-related cancer · 2026Article
- The pre-metastatic niche: mechanisms, heterogeneity, and therapeutic opportunities.Molecular cancer · 2026Review
- KCTD15 Enhances Stem Cell-Like Properties and Promotes Triple-Negative Breast Cancer Progression Through KLF4/β-Catenin Signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Emerging Protein Targets in Triple-Negative Breast Cancer: Beyond Conventional Therapy.Cancers · 2026Review
- Lipid metabolism reprogramming: key mechanism of breast cancer endocrine therapy resistance.Frontiers in oncology · 2026Review
- Cancer-associated adipocyte promote progression and immunosuppression in triple-negative breast cancer.Frontiers in oncology · 2026Article
- A lactylation-driven prognostic model for lung adenocarcinoma: cellular lactylation heterogeneity and immune insights.Translational lung cancer research · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
backgroundThe adipocyte-rich tumor microenvironment (TME) is recognized as a key factor in promoting cancer progression. A distinct characteristic of peritumoral adipocytes is their reduced lipid content and the acquisition of a proinflammatory phenotype. However, the underlying mechanisms by which adipocytes rewire metabolism and boost tumor progression in triple-negative breast cancer (TNBC) remain poorly understood.
methodsWe utilized transcriptomic analysis, bioinformatic analysis, metabolic flux analysis, protein-protein docking, gene and protein expression profiling, in vivo metastasis analysis and breast cancer specimens to explore how adipocytes reprogram tumor metabolism and progression in TNBC.
resultsOur findings reveal that Angiopoietin-like 4 (ANGPTL4) exhibits significantly higher expression levels in adipocyte-rich tumor circumstance compared to the symbiotic environment lacking of adipocyte. Furthermore, ANGPTL4 expression in tumor cells is essential for adipocyte-driven glycolysis and metastasis. Interleukin 6 (IL-6), enriched in cancer-associated adipocytes, and lipolysis-derived free fatty acids (FFAs) released from adipocytes, amplify ANGPTL4-mediated glycolysis and metastasis through activation of STAT3 and PPARα pathways in TNBC cells. Additionally, ANGPTL4 interacts with transcription factor KLF4 and enhances KLF4 activity, which further drives glycolysis and metastasis, whereas KLF4 knockdown attenuates migration and glycolysis in TNBC cells. Importantly, Elevated ANGPTL4 and KLF4 expression was observed in metastatic breast cancer specimens compared to non-metastatic cases and was positively correlated with poor prognosis.
conclusionCollectively, our results uncover a complex metabolic interaction between adipocytes and TNBC cells that promotes tumor aggressiveness. ANGPTL4 emerges as a key mediator in this process, making it a promising therapeutic target to inhibit TNBC progression.
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