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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
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]
Total Authors: 8
Affiliation:
[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
Total Affiliations: 5
Document type: Journal article
Source: PLoS One; v. 6, n. 12 DEC 28 2011.
Web of Science Citations: 9
Abstract

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)

FAPESP's process: 98/14247-6 - Center for Research on Cell-Based Therapy
Grantee:Marco Antonio Zago
Support type: Research Grants - Research, Innovation and Dissemination Centers - RIDC