ArticleProceedings of the National Academy of Sciences of the United States of America2011
Galectin-3 (Gal-3) induced by leukemia microenvironment promotes drug resistance and bone marrow lodgment in chronic myelogenous leukemia.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 99 citations in OpenAlex.
- Prostate Cancer Biomarkers with a Focus on Galectin-3: Emerging Clinical and Therapeutic Implications.Current oncology (Toronto, Ont.) · 2026Review
- Drug resistance in chronic myeloid leukemia: the involvement of Galectin-1 and Galectin-3.Molecular biology reports · 2026Review
- Galectin-3 induces neurodevelopmental apical-basal polarity and regulates gyrification.Science advances · 2025Article
- Galectin-3 Release in the Bone Marrow Microenvironment Promotes Drug Resistance and Relapse in Acute Myeloid Leukemia.Life (Basel, Switzerland) · 2025Review
- Biological Cargo: Exosomes and their Role in Cancer Progression and Metastasis.Current topics in medicinal chemistry · 2025Review
- Galectins-1, -3 and -9 in leukemia: mechanistic insights and therapeutic translation.Frontiers in immunology · 2025Review
- Secretory MPP3 reinforce myeloid differentiation trajectory and amplify myeloid cell production.The Journal of experimental medicine · 2023 · on this mapArticle
- Galectin-1 and Galectin-3 in B-Cell Precursor Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2022Article
- Review
- Galectin Family Members: Emerging Novel Targets for Lymphoma Therapy?Frontiers in oncology · 2022Review
- Peptide vaccination activating Galectin-3-specific T cells offers a novel means to target Galectin-3-expressing cells in the tumor microenvironment.Oncoimmunology · 2022Article
- LncRNA-PAX8-AS1 Silencing Decreases Cell Viability, Enhances Apoptosis, and Suppresses Doxorubicin Resistance in Myeloid Leukemia via the miR-378g/ERBB2 Axis.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Overcoming Microenvironment-Mediated Chemoprotection through Stromal Galectin-3 Inhibition in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2021Article
- Cancer non-stem cells as a potent regulator of tumor microenvironment: a lesson from chronic myeloid leukemia.Molecular biomedicine · 2021Review
- EWSR1 overexpression is a pro-oncogenic event in multiple myeloma.International journal of hematology · 2021Article
- The nuclear export protein XPO1 - from biology to targeted therapy.Nature reviews. Clinical oncology · 2021Review
- Review
- When Glycosylation Meets Blood Cells: A Glance of the Aberrant Glycosylation in Hematological Malignancies.Reviews of physiology, biochemistry and pharmacology · 2021Review
- The vascular bone marrow niche influences outcome in chronic myeloid leukemiaHaematologica · 2020Article
- The Bone Marrow Niche - The Tumor Microenvironment That Ensures Leukemia Progression.Advances in experimental medicine and biology · 2020Review
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone marrow (BM) microenvironment (BMME) constitutes the sanctuary for leukemic cells. In this study, we investigated the molecular mechanisms for BMME-mediated drug resistance and BM lodgment in chronic myelogenous leukemia (CML). Gene-expression profile as well as signal pathway and protein analyses revealed that galectin-3 (Gal-3), a member of the β-gal-binding galectin family of proteins, was specifically induced by coculture with HS-5 cells, a BM stroma cell-derived cell line, in all five CML cell lines examined. It was also found that primary CML cells expressed high levels of Gal-3 in BM. Enforced expression of Gal-3 activated Akt and Erk, induced accumulation of Mcl-1, and promoted in vitro cell proliferation, multidrug resistance to tyrosine kinase inhibitors for Bcr-Abl and genotoxic agents as a result of impaired apoptosis induction, and chemotactic cell migration to HS-5-derived soluble factors in CML cell lines independently of Bcr-Abl tyrosine kinase. The conditioned medium from Gal-3-overexpressing CML cells promoted in vitro cell proliferation of CML cells and HS-5 cells more than did the conditioned medium from parental cells. Moreover, the in vivo study in a mice transplantation model showed that Gal-3 overexpression promoted the long-term BM lodgment of CML cells. These results demonstrate that leukemia microenvironment-specific Gal-3 expression supports molecular signaling pathways for disease maintenance in BM and resistance to therapy in CML. They also suggest that Gal-3 may be a candidate therapeutic target to help overcome BMME-mediated therapeutic resistance.
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