REVIEW article
Front. Immunol.
Sec. Inflammation
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1685266
This article is part of the Research TopicDecoding Chronic Inflammation: The Role of Immune Cell CommunicationView all articles
Galectins-1, -3 and -9 in Leukemia: Mechanistic Insights and Therapeutic Translation
Provisionally accepted
- 1Central Hospital Affiliated to Shandong First Medical University, Jinan, China
- 2Northwest University, Xi'an, China
- 3Shandong Junteng Medical Technology Co., LTD, Jinan, China
- 4The Second Hospital of Shandong University, Jinan, China
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Galectins, β-galactoside-binding proteins, function as key regulators in pathological transitions, bridging tissue homeostasis to oncogenesis and inflammation through intracellular and extracellular mechanisms. Notably, they play a pivotal role in the pathogenesis of leukemia by interacting with glycoconjugates to promote tumor progression. Among them, Galectin-1 (Gal-1), Gal-3, and Gal-9 have been associated with multiple leukemia subtypes, such as acute myeloid leukemia (AML), acute promyelocytic leukemia (APL), B-cell precursor acute lymphoblastic leukemia (BCP-ALL), adult T-cell leukemia (ATL), and chronic lymphocytic leukemia (CLL). These galectins contribute to leukemic cell survival by modulating extracellular matrix (ECM) interactions, suppressing anti-tumor immune responses, and promoting immune escape. Their involvement in sustaining leukemic proliferation and immune evasion highlights their potential as therapeutic targets. Recent advancements in the development of galectin inhibitors provide promising avenues to disrupt these oncogenic pathways. However, distinct galectin isoform pathologies across diseases require highly selective therapeutics, and substantial carbohydrate recognition domain (CRD) structural homology combined with conserved β-D-galactopyranoside-binding mechanisms complicates specific inhibitor design. This review summarizes galectin-mediated mechanisms in leukemia biology, evaluates the potential of galectin-targeted therapies and offers insights for the development of specific inhibitors of Gal-1, -3, and -9 to promote clinical management and treatment efficacy.
Keywords: galectin, Leukemia, diagnosis, molecular mechanism, inhibitors
Received: 13 Aug 2025; Accepted: 08 Sep 2025.
Copyright: © 2025 Feng, Wang, Zhang, Guo, Zhao and Cai. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Shaojie Feng, Central Hospital Affiliated to Shandong First Medical University, Jinan, China
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