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Published on: November 28, 2019
Galectin-8 alters immune microenvironment and promotes tumor progression
Yiting Wang1,2, Yufan Sun3, Hai Li1
1Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, Shanghai Institute of Digestive Disease, Renji Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai, China.
Galectin-8 (Gal-8), encoded by LGALS8 gene, is a unique member of the Galectin family with diverse biological functions, including tumor-modulating capabilities. Recently, evidence has accumulated supporting an essential role for Gal-8 in regulating innate and adaptive immunity, with high expression in tumors and other immune dysregulation diseases. This study reveals the role of Gal-8-induced tumor immunosuppression by analyzing animal models and clinical data of tumor-infiltrating cells. In Gal-8 expressing tumor, we found that suppressive immune cells, including Tregs and MDSCs, expanded while CD8+ cells decreased, providing direct evidence that Gal-8 regulates the tumor immune microenvironment. In addition, we not only analyzed the expression of Gal-8 in clinical samples of breast and colorectal cancer but also classified the tissue expression patterns. Further analysis revealed that Gal-8 correlates with lymph node metastasis and immunophenotyping. Consistent with animal experiments, our analysis of LGALS8 gene expression showed its negative association with infiltrated active CD8+ T cells and immune stimulatory modulators in cancers. Our study identified the potential prognostic and therapeutic value of Gal-8, and further research on developing corresponding targeted therapeutic strategies is awaited.
Galectin-8 (Gal-8), encoded by LGALS8 gene, is a unique member of the Galectin family with diverse biological functions, including tumor-modulating capabilities. Recently, evidence has accumulated supporting an essential role for Gal-8 in regulating innate and adaptive immunity, with high expression in tumors and other immune dysregulation diseases. This study reveals the role of Gal-8-induced tumor immunosuppression by analyzing animal models and clinical data of tumor-infiltrating cells. In Gal-8 expressing tumor, we found that suppressive immune cells, including Tregs and MDSCs, expanded while CD8+ cells decreased, providing direct evidence that Gal-8 regulates the tumor immune microenvironment. In addition, we not only analyzed the expression of Gal-8 in clinical samples of breast and colorectal cancer but also classified the tissue expression patterns. Further analysis revealed that Gal-8 correlates with lymph node metastasis and immunophenotyping. Consistent with animal experiments, our analysis of LGALS8 gene expression showed its negative association with infiltrated active CD8+ T cells and immune stimulatory modulators in cancers. Our study identified the potential prognostic and therapeutic value of Gal-8, and further research on developing corresponding targeted therapeutic strategies is awaited.
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