Abstract
Galectins are β-galactoside binding lectins that contain one or more carbohydrate recognition domains. As a consequence of sugar-binding properties, galectins exhibit a variety of interactions with glycoproteins, thus playing important roles in various pathological processes. A number of studies have shown roles of galectins in cancer. Galectin-7 is a prototype member of the galectin family implicated in epithelial stratification and cell migration. It can act as a potent dual regulator in different types of cancer. Galectin-7 may contribute either to neoplastic transformation and tumour progression through regulation of cell growth, cell cycle, angiogenesis, apoptosis and cell migration or may have a protective effect in cancer depending on the tissue type. A perusal of the literature indicates particular roles of galectin-7 in carcinomas and melanomas, while contributions await greater exploration in other types of cancers including sarcomas and leukemia. This review collectively summarizes available literature on expression and roles of galectin-7 in different cancers.
Highlights
Lectins are non-enzymatic and non-immunoglobulin proteins that bind carbohydrates with high specificity
Tandem repeat type galectins are characterized by two non-identical carbohydrate recognition domain (CRD), which are linked by a short linker peptide of up to 70 amino acids while chimera type galectin has both CRD as well as N-terminal domain (Leffler et al, 2004)
Galectin-7 transfectant cells were further shown to have elevated matrix metalloproteinases-9 (MMP-9) expression as compared to control transfectants (Demers et al, 2007). This induced elevated MMP-9 expression was found to be galectin-7 specific, as its expression was completely abolished on addition of β-lactose. All these findings collectively indicated that galectin-7 can modulate the malignant growth mediated via MMP-9 expression under in-vivo conditions
Summary
Lectins are non-enzymatic and non-immunoglobulin proteins that bind carbohydrates with high specificity. Negative staining of both proteins in cervical carcinoma patients, independently as well as synergistically showed significantly lower 5 year over OS rate as compared to tissues with positive staining as indicated by Kaplan -Meier survival analysis This finding was further supported by the evidence that elevated galectin-7 expression had been associated with improved outcomes after radiation therapy (Tsai et al, 2013). Different studies reported the induction of galectin-7 expression in human and murine lymphoma cells on treatment with 5-aza-2’-deoxycytidine, a demethylating drug (Moisan et al, 2003; Demers et al, 2009) Taken together, all these findings proposed the role of aberrant methylation in regulation of galectin-7 gene expression in malignant form of lymphomas. Study involving B16F1, a melanoma cell line, confirmed galectin-7 expression at tumour site and
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