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Galectin-3 protects human breast carcinoma cells against nitric oxide-induced apoptosis: implication of galectin-3 function during metastasis.

Authors
Moon, BK; Lee, YJ; Battle, P; Jessup, JM; Raz, A; Kim, HR
Citation
The American journal of pathology, 159(3):1055-1060, 2001
Journal Title
The American journal of pathology
ISSN
0002-94401525-2191
Abstract
Galectin-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.
MeSH terms
AnimalsAntigens, Differentiation/pharmacology*Antigens, Differentiation/physiologyApoptosis/drug effects*Apoptosis/physiology*Breast Neoplasms/complicationsBreast Neoplasms/pathologyBreast Neoplasms/physiopathology*Carcinoma/complicationsCarcinoma/pathologyCarcinoma/physiopathology*Carcinoma/secondaryCell Survival/drug effectsFemaleGalectin 3HumansIschemia/mortalityIschemia/physiopathologyLiver CirculationMiceMice, NudeNitric Oxide/physiology*Reperfusion Injury/physiopathologyTumor Cells, Cultured
DOI
10.1016/S0002-9440(10)61780-4
PMID
11549597
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Journal Papers > School of Medicine / Graduate School of Medicine > Anesthesiology & Pain Medicine
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