| Full text | |
| 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 |