Galectin-3 Inhibits Cancer Metastasis by Negatively Regulating Integrin β3 Expression

Am J Pathol. 2019 Apr;189(4):900-910. doi: 10.1016/j.ajpath.2018.12.005. Epub 2019 Jan 14.


Galectin-3 (Gal-3; gene LGALS3) is a member of the β-galactose-binding lectin family. Previous studies showed that Gal-3 is expressed in several tissues across species and functions as a regulator of cell proliferation, apoptosis, adhesion, and migration, thus affecting many aspects of events, such as angiogenesis and tumorigenesis. Although several reports have suggested that the level of Gal-3 expression correlates positively with tumor progression, herein we show that highly metastatic mouse melanoma B16/BL6 cells express less Gal-3 than B16 cells with a lower metastatic potential. It was found that overexpression of Gal-3 in melanoma cells in fact suppresses metastasis. In contrast, knocking out Gal-3 expression in cancer cells promoted cell aggregation mediated through interactions with platelets and fibrinogen in vitro and increased the number of metastatic foci in vivo. Thus, reduced Gal-3 expression results in the up-regulation of β3 integrin expression, and this contributes to metastatic potential. These findings indicate that changes of Gal-3 expression in cancer cells during tumor progression influence the characteristics of metastatic cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Cell Adhesion
  • Cell Proliferation
  • Galectin 3 / physiology*
  • Gene Expression Regulation, Neoplastic*
  • Humans
  • Integrin beta3 / genetics
  • Integrin beta3 / metabolism*
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / prevention & control*
  • Lung Neoplasms / secondary
  • Melanoma, Experimental / metabolism
  • Melanoma, Experimental / pathology
  • Melanoma, Experimental / prevention & control*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Nude
  • Neovascularization, Pathologic / prevention & control*


  • Galectin 3
  • Integrin beta3