On the role of Galectin 3 in the Tumor Microenvironment

It was reported that the level of secreted Galectin 3 (Gal-3) could be as high as 31- fold in the serum of cancer patients with breast, colorectal, lung, bladder, head and neck, thyroid, prostate, and melanoma, and that patients with metastatic disease have higher concentrations of circulating Gal-3 than those with localized tumors . Thus Gal-3 was suggested to be an emerging promoter of cancer metastasis. Gal-3 was shown to recognize and bind to nearly all cell-surface and extracellular matrix glyco-components that contain terminal galactose residues, including growth factor receptors such as EGFR, VEGFR, and TGF-βR to name a few/ This wide array of Gal-3 interactions, mediated solely by sugar recognition, indicates that Gal-3 is involved in regulating a myriad of activities during cancer development, progression, and metastasis, leading to its characterization as a “jack-of-all-trades in cancer”. A lthough the initial studies demonstrating the role of galectin-3 in tumor angiogenesis were reported more than a decade ago, in the recent years an increasing interest in this field confirms its significance. More studies are in order using different models to analyze the significance of galectin-3 on various steps of angiogenesis to get a more comprehensive knowledge of this potentially important and exciting field. In the bone micro environment will show the presence of a complex network of multiple soluble factors drives vicious cycles of highly destructive bone remodeling, and will report that Gal-3 a may be targeted. In bone metastasis patient samples.