Galectin-3 Regulates Integrin α2β1-mediated Adhesion to Collagen-I and -IV

Friedrichs, Jens; Manninen, Aki; Müller, Daniel J.; Helenius, Jonne

doi:10.1074/jbc.m803634200

Cited by 87 publications

(62 citation statements)

References 47 publications

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“…Gal3 has been reported to regulate cell-cell adhesion and other key homeostatic properties such as cell-matrix adhesion, proliferation, and differentiation by associating with N-cadherin, ␤1 integrin, epithelial growth factor receptor, and transforming growth factor ␤ receptor (32)(33)(34)(35)(36)(37)(38)(39). We observed that Gal3 association with Dsg2 is mediated by N-linked glycans on Dsg2 and that this lactose-sensitive interaction promotes Dsg2 stability at the cell surface and epithelial intercellular adhesion.…”

mentioning

confidence: 65%

Galectin-3 Regulates Desmoglein-2 and Intestinal Epithelial Intercellular Adhesion

Jiang

Rankin

Nava

et al. 2014

Journal of Biological Chemistry

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Background: Desmoglein-2 mediates intestinal epithelial intercellular adhesion. Results: Galectin-3 was identified to associate with the ectodomain of desmoglein-2 and inhibit the degradation of desmoglein-2 and enhance intercellular adhesion. Conclusion: Galectin-3 lattices stabilize desmoglein-2 at the cell surface to regulate intercellular adhesion in intestinal epithelial cells. Significance: This study identifies a novel role of galectin-3 in controlling desmosome structure and function.

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mentioning

confidence: 65%

Galectin-3 Regulates Desmoglein-2 and Intestinal Epithelial Intercellular Adhesion

Jiang

Rankin

Nava

et al. 2014

Journal of Biological Chemistry

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“…Our liver-aggressive cells also showed an enhanced ability to interact with type IV collagen. The a 2 b 1 -integrin, which can interact with type IV collagen (Magro et al, 1997;Friedrichs et al, 2008), has been associated with gastric cancer carcinoma lymph node and liver metastasis (Ura et al, 1998). The use of an antagonist of a 2 b 1 has been reported to decrease the extravasation into the liver and micrometastasis associated with colorectal and hepatocellular carcinoma cell lines (Rosenow et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Claudin-2 is selectively enriched in and promotes the formation of breast cancer liver metastases through engagement of integrin complexes

et al. 2010

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The liver represents the third most frequent site of metastasis in patients with breast cancer. We performed in vivo selection using 4T1 breast cancer cells to identify genes associated with the liver metastatic phenotype. Coincident with the loss of numerous tight-junctional proteins, we observe claudin-2 overexpression, specifically in liver-aggressive breast cancer cells. We further demonstrate that claudin-2 is both necessary and sufficient for the ability of 4T1 breast cancer cells to colonize and grow in the liver. The liver-aggressive breast cancer cells display a claudin-2-mediated increase in their ability to adhere to extracellular matrix (ECM) components, such as fibronectin and type IV collagen. Claudin-2 facilitates these cell/matrix interactions by increasing the cell surface expression of a 2 b 1 -and a 5 b 1 -integrin complexes in breast cancer cells. Indeed, claudin-2-mediated adhesion to fibronectin and type IV collagen can be blocked with neutralizing antibodies that target a 5 b 1 and a 2 b 1 complexes, respectively. Immunohistochemical analyses reveal that claudin-2, although weakly expressed in primary human breast cancers, is readily detected in all liver metastasis samples examined to date. Together, these results uncover novel roles for claudin-2 in promoting breast cancer adhesion to the ECM and define its importance during breast cancer metastasis to the liver.

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“…Thus Gal-3 does not seem to affect multiple types of cell proliferation in the adult SVZ. Apart from its proliferative role, Gal-3 is also known to act as an adhesion and de-adhesion molecule (Friedrichs et al, 2008) and its pattern of expression in the SVZ led us to study neuroblast migration. Furthermore, Gal-3 binds -galactoside residues on EGFR, laminin, 1 integrin, NCAM and tenascin, all of which influence SVZ neuroblast migration (Aguirre et al, 2005;Cremer et al, 1994;Emsley and Hagg, 2003;Ghashghaei et al, 2007;Kim et al, 2009).…”

Section: Gal-3 Maintains Normal Svz Neuroblast Migrationmentioning

confidence: 99%

Galectin-3 maintains cell motility from the subventricular zone to the olfactory bulb

Comte

Kim

Young

et al. 2011

Journal of Cell Science

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The adult brain subventricular zone (SVZ) produces neuroblasts that migrate through the rostral migratory stream (RMS) to the olfactory bulb (OB) in a specialized niche. Galectin-3 (Gal-3) regulates proliferation and migration in cancer and is expressed by activated macrophages after brain injury. The function of Gal-3 in the normal brain is unknown, but we serendipitously found that it was expressed by ependymal cells and SVZ astrocytes in uninjured mice. Ependymal cilia establish chemotactic gradients and astrocytes form glial tubes, which combine to aid neuroblast migration. Whole-mount preparations and electron microscopy revealed that both ependymal cilia and SVZ astrocytes were disrupted in Gal3−/− mice. Interestingly, far fewer new BrdU+ neurons were found in the OB of Gal3−/− mice, than in wild-type mice 2 weeks after labeling. However, SVZ proliferation and cell death, as well as OB differentiation rates were unaltered. This suggested that decreased migration in vivo was sufficient to decrease the number of new OB neurons. Two-photon time-lapse microscopy in forebrain slices confirmed decreased migration; cells were slower and more exploratory in Gal3−/− mice. Gal-3 blocking antibodies decreased migration and dissociated neuroblast cell–cell contacts, whereas recombinant Gal-3 increased migration from explants. Finally, we showed that expression of phosphorylated epidermal growth factor receptor (EGFR) was increased in Gal3−/− mice. These results suggest that Gal-3 is important in SVZ neuroblast migration, possibly through an EGFR-based mechanism, and reveals a role for this lectin in the uninjured brain.

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Galectin-3 Regulates Integrin α2β1-mediated Adhesion to Collagen-I and -IV

Cited by 87 publications

References 47 publications

Galectin-3 Regulates Desmoglein-2 and Intestinal Epithelial Intercellular Adhesion

Galectin-3 Regulates Desmoglein-2 and Intestinal Epithelial Intercellular Adhesion

Claudin-2 is selectively enriched in and promotes the formation of breast cancer liver metastases through engagement of integrin complexes

Galectin-3 maintains cell motility from the subventricular zone to the olfactory bulb

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