Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2024 Jan 27;15(6):1675-1686.
doi: 10.7150/jca.90457. eCollection 2024.

Inside anticancer therapy resistance and metastasis. Focus on CD36

Affiliations
Review

Inside anticancer therapy resistance and metastasis. Focus on CD36

Ioana M Lambrescu et al. J Cancer. .

Abstract

Despite recent advances in targeted cancer therapies, drug resistance remains an important setback in tumor control. Understanding the complex mechanisms involved in both innate and acquired drug resistance represents the first step in discovering novel therapeutic agents. Because of its importance in tumorigenesis, progression, and metastasis, lipid metabolism is increasingly garnering attention. CD36 is a membrane receptor at the top of the signaling cascade that transports lipids. Its expression has been repeatedly presented as an unfavorable prognostic factor for various tumor types, raising the question: could CD36 be a critical factor in cancer treatment resistance? In our review, we set out to explore the most prominent studies on the implication of CD36 in resistance to platinum-based drugs and other adjuvant cancer therapies in solid and haematological neoplasia. Moreover, we provide an overview of the latest anti-CD36 cancer therapies, thus opening new perspectives for future personalized medicine.

Keywords: CD36; cancer treatment; chemotherapy; drug resistance; lipid metabolism.

PubMed Disclaimer

Conflict of interest statement

Competing Interests: The authors have declared that no competing interest exists.

Figures

Figure 1
Figure 1
The most significant historical milestones of CD36. Created with BioRender.com
Figure 2
Figure 2
CD36 contributes to the growth and spread of tumors by boosting lipid absorption and fatty acid (FA) oxidation. Several proteins, notably fatty acid binding protein (FABP) and fatty acyl-CoA desaturases (FADS), coordinate tumor cell development. As seen on the right side of the picture, lipid metabolism alterations may also affect cell motility, which may ultimately lead to metastasis. Several enzymes, including ATP citrate lyase (ACLY), carnitine palmitoyl transferase 1 (CTP-1), acetyl-CoA carboxylase (ACC), and fatty acid synthase (FASN), are involved in this process. In addition, FA are synthesized from scratch, and FASN is overexpressed in a range of cancer types. Created with BioRender.com

References

    1. Wang J, Li Y. CD36 tango in cancer: Signaling pathways and functions. Theranostics. 2019;9(17):4893–908. - PMC - PubMed
    1. Silverstein RL, Febbraio M. CD36, a scavenger receptor involved in immunity, metabolism, angiogenesis, and behavior. Sci Signal. 2009 May;2(72):re3. - PMC - PubMed
    1. Pascual G, Avgustinova A, Mejetta S, Martín M, Castellanos A, Attolini CSO. et al. Targeting metastasis-initiating cells through the fatty acid receptor CD36. Nature [Internet] 2017;541(7635):41–5. Available from: http://dx.doi.org/10.1038/nature20791. - PubMed
    1. Clemetson KJ, Pfueller SL, Luscher EF, Jenkins CSP. Isolation of the membrane glycoproteins of human blood platelets by lectin affinity chromatography. BBA - Biomembr. 1977;464(3):493–508. - PubMed
    1. Lehner R, Quiroga AD. Fatty Acid Handling in Mammalian Cells. In: Biochemistry of Lipids, Lipoproteins and Membranes [Internet] Elsevier. 2016. p. 149-84. Available from: https://linkinghub.elsevier.com/retrieve/pii/B9780444634382000055.