CD36: The Bridge between Lipids and Tumors

Molecules. 2024 Jan 21;29(2):531. doi: 10.3390/molecules29020531.

Abstract

It has been found that the development of some cancers can be attributed to obesity, which is associated with the excessive intake of lipids. Cancer cells undergo metabolic reprogramming, shifting from utilizing glucose to fatty acids (FAs) for energy. CD36, a lipid transporter, is highly expressed in certain kinds of cancer cells. High expressions of CD36 in tumor cells triggers FA uptake and lipid accumulation, promoting rapid tumor growth and initiating metastasis. Meanwhile, immune cells in the tumor microenvironment overexpress CD36 and undergo metabolic reprogramming. CD36-mediated FA uptake leads to lipid accumulation and has immunosuppressive effects. This paper reviews the types of FAs associated with cancer, high expressions of CD36 that promote cancer development and progression, effects of CD36 on different immune cells in the tumor microenvironment, and the current status of CD36 as a therapeutic target for the treatment of tumors with high CD36 expression.

Keywords: CD36; fatty acid; immunosuppress; lipid; metastasis-initiating cells.

Publication types

  • Review

MeSH terms

  • Biological Transport
  • CD36 Antigens / genetics
  • CD36 Antigens / metabolism
  • Fatty Acids / metabolism
  • Humans
  • Neoplasms*
  • Obesity
  • Tumor Microenvironment

Substances

  • Fatty Acids
  • CD36 Antigens