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  • Inhibiting galectin-1 reduces murine lung metastasis with increased CD4+ and CD8+ T cells and reduced cancer cell adherence

    Author(s)
    Ito, Koichi
    Ralph, Stephen J
    Griffith University Author(s)
    Ralph, Stephen J.
    Year published
    2012
    Metadata
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    Abstract
    Galectin-1 is a beta-galactoside-binding protein overexpressed by cancer cells. The primary roles of galectin-1 in cancer progression and metastasis are attributed to suppression of T cell immune responses, promotion of tumor angiogenesis and increased tumor cell adhesion and invasion. Using pulmonary metastasis models of murine breast (4T1) and colon (CT26) cancer, we demonstrate that targeting galectin-1 with thiodigalactoside (TDG) or shRNA galectin-1 knockdown (G1KD) results in a significant reduction in lung metastasis. Increased numbers of CD4+ helper T cells and CD8+ cytotoxic T lymphocytes were found in ...
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    Galectin-1 is a beta-galactoside-binding protein overexpressed by cancer cells. The primary roles of galectin-1 in cancer progression and metastasis are attributed to suppression of T cell immune responses, promotion of tumor angiogenesis and increased tumor cell adhesion and invasion. Using pulmonary metastasis models of murine breast (4T1) and colon (CT26) cancer, we demonstrate that targeting galectin-1 with thiodigalactoside (TDG) or shRNA galectin-1 knockdown (G1KD) results in a significant reduction in lung metastasis. Increased numbers of CD4+ helper T cells and CD8+ cytotoxic T lymphocytes were found in the peripheral blood of both TDGtreated and G1KD cell challenged mice. The levels of TUNEL+ apoptotic cancer cells and the presence of CD3+ T cells were also increased in lung metastases. Furthermore, galectin-1 was found to bind to the adhesion molecules, CD44 and CD326, which are also known as markers of breast and colon cancer stem cells, and TDG likely blocks galectin-1 binding to these molecules. The TDGmediated inhibition of galectin-1 binding reduced 4T1 cell adhesion to the basement membrane protein laminin, Matrigel and EAhy926 endothelial cell surfaces. These findings establish possible mechanisms for the anti-metastatic effect of galectin-1 inhibition and suggest that targeting galectin-1 may represent a promising and effective anti-metastatic therapy.
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    Journal Title
    Clinical & Experimental Metastasis
    Volume
    29
    Issue
    6
    DOI
    https://doi.org/10.1007/s10585-012-9471-7
    Subject
    Clinical sciences
    Oncology and carcinogenesis
    Cancer therapy (excl. chemotherapy and radiation therapy)
    Publication URI
    http://hdl.handle.net/10072/46121
    Collection
    • Journal articles

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