Galectin-9, a pro-survival factor inducing immunosuppression, leukemic cell transformation and expansion

• Published in: Molecular biology reports 2024-12, Vol.51 (1), p.571-571, Article 571
• Main Author: Yıldırım, Cansu
• Format: Article
• Language: English
• Subjects: Animal Anatomy; Animal Biochemistry; Animals; Biomedical and Life Sciences; Blast cells; Cell Proliferation; Cell Transformation, Neoplastic - genetics; Cell Transformation, Neoplastic - immunology; Disease resistance; Drug resistance; Effector cells; Galectin-9; Galectins - metabolism; Hepatitis A Virus Cellular Receptor 2 - metabolism; Histology; Humans; Immune checkpoint; Immune evasion; Immune response; Immune Tolerance; Immunosuppression; Immunosurveillance; Immunotherapy; Killer Cells, Natural - immunology; Killer Cells, Natural - metabolism; Leukemia; Leukemia - immunology; Leukocytes; Life Sciences; Lymphocytes T; Malignancy; Medical prognosis; Molecular modelling; Morphology; Review; Signal Transduction; Survival factor; Tumor Escape
• ISSN: 0301-4851; 1573-4978
• DOI: 10.1007/s11033-024-09563-w

Leukemia is a malignancy of the bone marrow and blood originating from self-renewing cancerous immature blast cells or transformed leukocytes. Despite improvements in treatments, leukemia remains still a serious disease with poor prognosis because of disease heterogeneity, drug resistance and relapse. There is emerging evidence that differentially expression of co-signaling molecules play a critical role in tumor immune evasion. Galectin-9 (Gal-9) is one of the key proteins that leukemic cells express, secrete, and use to proliferate, self-renew, and survive. It also suppresses host immune responses controlled by T and NK cells, enabling leukemic cells to evade immune surveillance. The present review provides the molecular mechanisms of Gal-9-induced immune evasion in leukemia. Understanding the complex immune evasion machinery driven by Gal-9 expressing leukemic cells will enable the identification of novel therapeutic strategies for efficient immunotherapy in leukemic patients. Combined treatment approaches targeting T-cell immunoglobulin and mucin domain-3 (Tim-3)/Gal-9 and other immune checkpoint pathways can be considered, which may enhance the efficacy of host effector cells to attack leukemic cells.