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<p>Fatty acid metabolism is a core metabolic pathway regulating tumor metastasis. Through fatty acid uptake and intracellular transport mediated by CD36 and fatty acid-binding proteins (FABPs), fatty acid oxidation (FAO) regulated by carnitine palmitoyltransferase 1 (CPT1), and fatty acid desaturation modification mediated by stearoyl-CoA desaturase 1 (SCD1) and fatty acid desaturase 2 (FADS2), it modulates the entire process of tumor cell invasion, circulatory survival and distal colonization from the perspectives of membrane lipid remodeling, energy homeostasis and signal transduction. The metabolic heterogeneity of cancer stem cells (CSCs) and epithelial-mesenchymal transition (EMT)-like cells, as well as the metabolic reprogramming mediated by the target organ microenvironment, further enhance metastatic plasticity and organotropism. Interventional strategies targeting key molecules of fatty acid metabolism have shown promising anti-metastatic potential, providing a core research direction for subsequent precise metabolic targeted therapy against metastasis.</p>

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Mechanisms of fatty acid metabolism in tumor metastasis and targeted therapeutic strategies

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月29日

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  • Jiaqi Zhou,
  • Chengwang Guo,
  • Jiaying Li,
  • Xueting Xia,
  • Zhaojuan Bai,
  • Shuping Li,
  • Yongjin Wang,
  • Xiaojun Liu

摘要

Fatty acid metabolism is a core metabolic pathway regulating tumor metastasis. Through fatty acid uptake and intracellular transport mediated by CD36 and fatty acid-binding proteins (FABPs), fatty acid oxidation (FAO) regulated by carnitine palmitoyltransferase 1 (CPT1), and fatty acid desaturation modification mediated by stearoyl-CoA desaturase 1 (SCD1) and fatty acid desaturase 2 (FADS2), it modulates the entire process of tumor cell invasion, circulatory survival and distal colonization from the perspectives of membrane lipid remodeling, energy homeostasis and signal transduction. The metabolic heterogeneity of cancer stem cells (CSCs) and epithelial-mesenchymal transition (EMT)-like cells, as well as the metabolic reprogramming mediated by the target organ microenvironment, further enhance metastatic plasticity and organotropism. Interventional strategies targeting key molecules of fatty acid metabolism have shown promising anti-metastatic potential, providing a core research direction for subsequent precise metabolic targeted therapy against metastasis.