The Promigratory Activity of the Matricellular Protein Galectin-3 Depends on the Activation of PI-3 Kinase

Autor(es)

Melo, Fabiana H. M. ^[1] ; Butera, Diego ^{[2, 1]} ; Junqueira, Mara de Souza ^[1] ; Hsu, Daniel K. ^[3] ; Moura da Silva, Ana Maria ^[2] ; Liu, Fu-Tong ^[3] ; Santos, Marinilice F. ^[4] ; Chammas, Roger ^{[1, 5]}

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Fac Med, Dept Radiol & Oncol, Sao Paulo - Brazil

^[2] Inst Butantan, Lab Imunopatol, Sao Paulo - Brazil

^[3] Univ Calif Davis, Dept Dermatol, Davis, CA 95616 - USA

^[4] Univ Sao Paulo, Inst Ciencias Biomed, Dept Biol Celular & Desenvolvimento, BR-05508 Sao Paulo - Brazil

^[5] Inst Canc Estado Sao Paulo, Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: PLoS One; v. 6, n. 12 DEC 28 2011.
• Citações Web of Science: 9

Resumo

Expression of galectin-3 is associated with sarcoma progression, invasion and metastasis. Here we determined the role of extracellular galectin-3 on migration of sarcoma cells on laminin-111. Cell lines from methylcholanthrene-induced sarcomas from both wild type and galectin-3(-/-) mice were established. Despite the presence of similar levels of laminin-binding integrins on the cell surface, galectin-3(-/-) sarcoma cells were more adherent and less migratory than galectin-3+/+ sarcoma cells on laminin-111. When galectin-3 was transiently expressed in galectin-3(-/-) sarcoma cells, it inhibited cell adhesion and stimulated the migratory response to laminin in a carbohydrate-dependent manner. Extracellular galectin-3 led to the recruitment of SHP-2 phosphatase to focal adhesion plaques, followed by a decrease in the amount of phosphorylated FAK and phospho-paxillin in the lamellipodia of migrating cells. The promigratory activity of extracellular galectin-3 was inhibitable by wortmannin, implicating the activation of a PI-3 kinase dependent pathway in the galectin-3 triggered disruption of adhesion plaques, leading to sarcoma cell migration on laminin-111. (AU)

• Processo FAPESP: 98/14247-6 - Center for Research on Cell-Based Therapy
• Beneficiário: Marco Antonio Zago
• Modalidade de apoio: Auxílio à Pesquisa - Centros de Pesquisa, Inovação e Difusão - CEPIDs