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pubmed-article:11549597pubmed:abstractTextGalectin-3 is a beta-galactoside-binding protein which regulates many biological processes including cell adhesion, migration, cell growth, tumor progression, metastasis, and apoptosis. Although the exact function of galectin-3 in cancer development is unclear, galectin-3 expression is associated with neoplastic progression and metastatic potential. Since studies have suggested that tumor cell survival in microcirculation determines the metastatic outcome, we examined the effect of galectin-3 overexpression in human breast carcinoma cell survival using the liver ischemia/reperfusion metastasis model. While the majority of control cells died by hepatic ischemia/reoxygenation, nearly all of galectin-3 overexpressing cells survived. We showed that galectin-3 inhibits nitrogen free radical-mediated apoptosis, one of the major death pathways induced during hepatic ischemia/reperfusion. Galectin-3 inhibition of apoptosis involved protection of mitochondrial integrity, inhibition of cytochrome c release and caspase activation. Taking these results together with the previous observation that galectin-3 inhibits apoptosis induced by loss of cell adhesion, we propose that galectin-3 is a critical determinant for anchorage-independent and free radical-resistant cell survival during metastasis.lld:pubmed
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pubmed-article:11549597pubmed:authorpubmed-author:JessupJ MJMlld:pubmed
pubmed-article:11549597pubmed:authorpubmed-author:LamK BKBlld:pubmed
pubmed-article:11549597pubmed:authorpubmed-author:LeeY JYJlld:pubmed
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pubmed-article:11549597pubmed:dateRevised2009-11-18lld:pubmed
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pubmed-article:11549597pubmed:articleTitleGalectin-3 protects human breast carcinoma cells against nitric oxide-induced apoptosis: implication of galectin-3 function during metastasis.lld:pubmed
pubmed-article:11549597pubmed:affiliationDepartment of Anesthesiology, Ajou University School of Medicine, Suwon, Korea.lld:pubmed
pubmed-article:11549597pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11549597pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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