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Galectin-1 (Gal-1), a carbohydrate-binding protein whose secretion is enhanced by hypoxia, promotes tumor aggressiveness by promoting angiogenesis and T-cell apoptosis. However, the importance of tumor versus host Gal-1 in tumor progression is undefined. Here we offer evidence that implicates tumor Gal-1 and its modulation of T-cell immunity in progression. Comparing Gal-1-deficient mice as hosts for Lewis lung carcinoma cells where Gal-1 levels were preserved or knocked down, we found that tumor Gal-1 was more critical than host Gal-1 in promoting tumor growth and spontaneous metastasis. Enhanced growth and metastasis associated with Gal-1 related to its immunomodulatory function, insofar as the benefits of Gal-1 expression to Lewis lung carcinoma growth were abolished in immunodeficient mice. In contrast, angiogenesis, as assessed by microvessel density count, was similar between tumors with divergent Gal-1 levels when examined at a comparable size. Our findings establish that tumor rather than host Gal-1 is responsible for mediating tumor progression through intratumoral immunomodulation, with broad implications in developing novel targeting strategies for Gal-1 in cancer.

Original publication

DOI

10.1158/0008-5472.CAN-10-4157

Type

Journal article

Journal

Cancer Res

Publication Date

01/07/2011

Volume

71

Pages

4423 - 4431

Keywords

Animals, Apoptosis, Carcinoma, Lewis Lung, Cell Growth Processes, Galectin 1, Gene Knockdown Techniques, Humans, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Mice, Inbred NOD, Mice, SCID, Neoplasm Metastasis, T-Lymphocytes