Journal
CELLULAR IMMUNOLOGY
Volume 333, Issue -, Pages 34-45Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.cellimm.2018.03.008
Keywords
Galectins; Tumor microenvironment; Fibroblasts; Endothelial cells; Immune cells
Categories
Funding
- Argentinean Agency for Promotion of Science and Technology [PICT-2012-2440, PICT-V-2014-3687, PICT-2007-1631, PICT-2012-0071]
- Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET)
- University of Buenos Aires
- Sales Foundation
- Kenneth Rainin Foundation
- Excellence Award of the American Association of Immunologists
- Bunge and Born Foundation
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Tumor cells corrupt surrounding normal cells instructing them to support proliferative, pro-angiogenic and immunosuppressive networks that favor tumorigenesis and metastasis. This dynamic cross-talk is sustained by a range of intracellular signals and extracellular mediators produced by both tumoral and non-tumoral cells. Galectins-whether secreted or intracellularly expressed- play central roles in the tumorigenic process by delivering regulatory signals that contribute to reprogram fibroblasts, endothelial and immune cell programs. Through glycosylation-dependent or independent mechanisms, these endogenous lectins control a variety of cellular events leading to tumor cell proliferation, survival, migration, inflammation, angiogenesis and immune escape. Here we discuss the role of galectin-driven pathways, particularly those activated in non-tumoral stromal cells, in modulating tumor progression.
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