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Phenotype-specific melanoma uptake of fatty acid from human adipocytes activates AXL and CAV1-dependent β-catenin

Ana Chocarro-Calvo, Miguel Jociles-Ortega, José Manuel García-Martinez

Biorxiv : the Preprint Server for Biology

|February 8, 2024

Summary

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This summary is machine-generated.

Melanoma cells with low MITF expression drive fat breakdown and absorb fatty acids independently of FATP. Oleic acid reprograms these cells to a highly invasive state via AXL activation.

Area of Science:

Oncology
Cancer Biology
Metabolism

Background:

Tumor microenvironment interactions drive cancer progression and therapy resistance.
Nutrient availability influences cancer cell phenotype, but specific nutrient effects on distinct phenotypes are unclear.
Melanoma exhibits phenotypic diversity, impacting disease outcomes.

Approach:

Investigated nutrient-driven phenotypic changes in melanoma using adipocytes.
Examined the uptake and utilization of adipocyte-derived free fatty acids by melanoma cells.
Assessed the role of oleic acid and AXL signaling in melanoma cell invasion and reprogramming.

Key Points:

MITF^Low melanoma cells, not MITF^High cells, induce lipolysis in adipocytes.
MITF^Low cells uptake free fatty acids independently of fatty acid transporter (FATP).

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Oleic acid reprograms MITF^Low cells to an invasive phenotype via AXL activation, driving SRC-dependent β-catenin-CAV1 complex formation.

Conclusions:

Specific nutrient inputs, like oleic acid, can activate phenotype-specific pro-metastasis programs in melanoma.
AXL activation by oleic acid promotes invasion and nuclear translocation of a β-catenin-CAV1 complex.
Findings suggest implications for FATP-targeted therapies in managing melanoma metastasis.