ArticleGenes & development2025
Fatty acid uptake activates an AXL-CAV1-β-catenin axis to drive melanoma progression.
Article in Genes & development, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
9 citing papers in PubMed.
- MITF-Driven melanoma plasticity as a core mechanism of therapy resistance: integrating microenvironmental signaling, mechanotransduction, and metabolic reprogramming.Cell cycle (Georgetown, Tex.) · 2026Review
- AXL is associated with STAT3 activation in breast cancer.Molecular and clinical oncology · 2026Article
- Plasma exosomal fibroblast activation protein: a novel biomarker links fatty acid metabolic dysregulation to systemic lupus erythematosus.Arthritis research & therapy · 2026Article
- Glycosylated extracellular vesicles drive a metabolic interplay between gastric cancer cells and adipocytes.Extracellular vesicles and circulating nucleic acids · 2026Article
- The SPA17-AXL axis drives melanoma aggressiveness and SPA17-targeting vaccination exhibits antitumor efficacy.Frontiers in immunology · 2026Article
- MITF, TFEB, and TFE3 drive distinct adaptive gene expression programs and immune infiltration in melanoma.Cell reports · 2025Article
- Two Faces of Greater Omentum.Comprehensive physiology · 2025Review
- From fat to fear: how lipid powers cancer spread.Genes & development · 2025Review
- Solute carrier protein family: physiological functions, disease associations, and therapeutic potential in immune-related disorders.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Interaction between the tumor microenvironment and cancer cell plasticity drives intratumor phenotypic heterogeneity and underpins disease progression and nongenetic therapy resistance. Phenotype-specific expression of the AXL receptor tyrosine kinase is a pivotal player in dormancy, invasion, and resistance to treatment. However, although the AXL ligand GAS6 is present within tumors, how AXL is activated in metastasizing cells remains unclear. Here, using melanoma as a model, we reveal that AXL is activated by exposure to human adipocytes and to oleic acid, a monounsaturated fatty acid abundant in lymph and in adipocytes. AXL activation triggers SRC-dependent formation and nuclear translocation of a β-catenin-CAV1 complex required for melanoma invasiveness. Remarkably, only undifferentiated AXL
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Registered trials
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