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 Sep;82(3):1735-1750.
doi: 10.1007/s12013-024-01350-5. Epub 2024 Jun 17.

Detailed role of SR-A1 and SR-E3 in tumor biology, progression, and therapy

Mohamed J Saadh  1 , Harikumar Pallathadka  2 , Hussein Salim Abed  3 , Soumya V Menon  4 , G V Sivaprasad  5 , Ahmed Hjazi  6 , Jasur Rizaev  7 , Sahil Suri  8 , Mohammed Abed Jawad  9 , Beneen Husseen  10   11   12
Affiliations
Review

Detailed role of SR-A1 and SR-E3 in tumor biology, progression, and therapy

Mohamed J Saadh et al. Cell Biochem Biophys. 2024 Sep.

Abstract

The first host defense systems are the innate immune response and the inflammatory response. Among innate immune cells, macrophages, are crucial because they preserve tissue homeostasis and eradicate infections by phagocytosis, or the ingestion of particles. Macrophages exhibit phenotypic variability contingent on their stimulation state and tissue environment and may be detected in several tissues. Meanwhile, critical inflammatory functions are played by macrophage scavenger receptors, in particular, SR-A1 (CD204) and SR-E3 (CD206), in a variety of pathophysiologic events. Such receptors, which are mainly found on the surface of multiple types of macrophages, have different effects on processes, including atherosclerosis, innate and adaptive immunity, liver and lung diseases, and, more recently, cancer. Although macrophage scavenger receptors have been demonstrated to be active across the disease spectrum, conflicting experimental findings and insufficient signaling pathways have hindered our comprehension of the molecular processes underlying its array of roles. Herein, as SR-A1 and SR-E3 functions are often binary, either protecting the host or impairing the pathophysiology of cancers has been reviewed. We will look into their function in malignancies, with an emphasis on their recently discovered function in macrophages and the possible therapeutic benefits of SR-A1 and SR-E3 targeting.

Keywords: Cancer; Macrophages; SR-A1; SR-E3; Therapy.

PubMed Disclaimer

Similar articles

See all similar articles

References

    1. Maiorino, L., Daßler-Plenker, J., Sun, L., & Egeblad, M. (2022). Innate immunity and cancer pathophysiology. Annual Review of Pathology, 17, 425–457. - PubMed - DOI
    1. Mulder, W. J. M., Ochando, J., Joosten, L. A. B., Fayad, Z. A., & Netea, M. G. (2019). Therapeutic targeting of trained immunity. Nature Reviews Drug Discovery, 18, 553–566. - PubMed - PMC - DOI
    1. Xia, L., Oyang, L., Lin, J., Tan, S., Han, Y., & Wu, N. et al. (2021). The cancer metabolic reprogramming and immune response. Molecular Cancer, 20, 28. - PubMed - PMC - DOI
    1. Xiang, X., Wang, J., Lu, D., & Xu, X. (2021). Targeting tumor-associated macrophages to synergize tumor immunotherapy. Signal Transduction And Targeted Therapy, 6, 75. - PubMed - PMC - DOI
    1. Zhang, H., Liu, L., Liu, J., Dang, P., Hu, S., & Yuan, W. et al. (2023). Roles of tumor-associated macrophages in anti-PD-1/PD-L1 immunotherapy for solid cancers. Molecular Cancer, 22, 58. - PubMed - PMC - DOI

LinkOut - more resources