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Abstract
Evasion of immune surveillance is an accepted hallmark of tumor progression. The production of immune suppressive mediators by tumor cells is one of the major mechanisms of tumor immune escape. Galectin-1 (Gal-1), a pivotal immunosuppressive molecule, is expressed by many types of cancer. Tumor-secreted Gal-1 can bind to glycosylated receptors on immune cells and trigger the suppression of immune cell function in the tumor microenvironment, contributing to the immune evasion of tumors. The aim of this review is to summarize the current literature on the expression and function of Gal-1 in the human tumor microenvironment, as well as therapeutics targeting Gal-1.
Highlights
Chawla et al found that moderate to marked lymphocyte infiltrates were present in 58.8% of the Head and Neck Cancer (HNC) patient cohort, including T cells, B cells, and FoxP3-expressing T cells, while Gal-1 staining within lymphocyte areas of the tumor was significantly associated with poorer patient outcomes [45]
We have summarized the role of tumor-derived Gal-1 in tumor immune escape
No FDA-approved Gal-1 targeting agents are available in clinics, despite convincing experimental and pre-clinical data supporting the clear role of Gal-1 in cancer progression
Summary
Carbohydrate interactions on the GBP cell surface play key roles in immune responses and in the tumor microenvironment [5]. In 1975, Teichberg et al discovered electrolectin from the electric eel (Electrophorus electricus) [7] It was the first vertebrate galectin, Galectin-1 (Gal-1). Galectins have a broad spectrum of effects on diverse immune cells, promoting inflammation or inhibiting immune responses mediated by T-cells and dependent on the receptors in specific target cells [11]. Gal-1 has been known to promote cancer cell growth; in addition, tumor-secreted Gal-1 is involved in immune escape by tumors, indicating that Gal-1 is a critical molecular target in cancer and could be a potentially therapeutic target for cancer treatment
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