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- W2049463500 abstract "Galectin-1 (Gal-1)-binding to Gal-1 ligands on immune and endothelial cells can influence melanoma development through dampening antitumor immune responses and promoting angiogenesis. However, whether Gal-1 ligands are functionally expressed on melanoma cells to help control intrinsic malignant features remains poorly understood. Here, we analyzed expression, identity, and function of Gal-1 ligands in melanoma progression. Immunofluorescent analysis of benign and malignant human melanocytic neoplasms revealed that Gal-1 ligands were abundant in severely dysplastic nevi, as well as in primary and metastatic melanomas. Biochemical assessments indicated that melanoma cell adhesion molecule (MCAM) was a major Gal-1 ligand on melanoma cells that was largely dependent on its N-glycans. Other melanoma cell Gal-1 ligand activity conferred by O-glycans was negatively regulated by α2,6 sialyltransferase ST6GalNAc2. In Gal-1-deficient mice, MCAM-silenced (MCAM(KD)) or ST6GalNAc2-overexpressing (ST6(O/E)) melanoma cells exhibited slower growth rates, underscoring a key role for melanoma cell Gal-1 ligands and host Gal-1 in melanoma growth. Further analysis of MCAM(KD) or ST6(O/E) melanoma cells in cell migration assays indicated that Gal-1 ligand-dependent melanoma cell migration was severely inhibited. These findings provide a refined perspective on Gal-1/melanoma cell Gal-1 ligand interactions as contributors to melanoma malignancy." @default.
- W2049463500 created "2016-06-24" @default.
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- W2049463500 date "2015-07-01" @default.
- W2049463500 modified "2023-10-18" @default.
- W2049463500 title "Melanoma Cell Galectin-1 Ligands Functionally Correlate with Malignant Potential" @default.
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- W2049463500 doi "https://doi.org/10.1038/jid.2015.95" @default.
- W2049463500 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4466041" @default.
- W2049463500 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25756799" @default.
- W2049463500 hasPublicationYear "2015" @default.
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