Ligand-dependent CD36 functions in cancer progression, metastasis, immune response, and drug resistance

• Published in: Biomedicine & pharmacotherapy 2023-12, Vol.168, p.115834-115834, Article 115834
• Main Authors: Xia, Liqun, Zhou, Zhenwei, Chen, Xianjiong, Luo, Wenqin, Ding, Lifeng, Xie, Haiyun, Zhuang, Wei, Ni, Kangxin, Li, Gonghui
• Format: Article
• Language: English
• Subjects: Cancer progression; CD36; Drug resistance; Immune response; Ligand-dependent function; Lipid uptake; Metastasis; Thrombospondin
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2023.115834

CD36, a multifunctional glycoprotein, has been shown to play critical roles in tumor initiation, progression, metastasis, immune response, and drug resistance. CD36 serves as a receptor for a wide range of ligands, including lipid-related ligands (e.g., long-chain fatty acid (LCFA), oxidized low-density lipoprotein (oxLDL), and oxidized phospholipids), as well as protein-related ligands (e.g., thrombospondins, amyloid proteins, collagens I and IV). CD36 is overexpressed in various cancers and may act as an independent prognostic marker. While it was initially identified as a mediator of anti-angiogenesis through its interaction with thrombospondin-1 (TSP1), recent research has highlighted its role in promoting tumor growth, metastasis, drug resistance, and immune suppression. The varied impact of CD36 on cancer is likely ligand-dependent. Therefore, we focus specifically on the ligand-dependent role of CD36 in cancer to provide a critical review of recent advances, perspectives, and challenges. •CD36, a multifunctional glycoprotein, serves as a receptor for a variety of ligands.•The role of CD36 in cancer varies depending on the binding of different ligands.•CD36-mediated lipid uptake enhances tumor progression and contributes to therapy resistance.•CD36 mediates TSP-induced anti-angiogenesis as well as invasion in cancers.