Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/33578
Title: Role of SOCS-1 Gene on Melanoma Cell Growth and Tumor Development
Authors: Borin Scutti, Jorge Augusto [UNIFESP]
Matsuo, Alisson Leonardo [UNIFESP]
Pereira, Felipe Valença [UNIFESP]
Massaoka, Mariana Hiromi [UNIFESP]
Figueiredo, Carlos Rogerio [UNIFESP]
Moreira, Dayson Friaca
Belizario, Jose Ernesto
Travassos, Luiz Rodolpho [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Universidade de São Paulo (USP)
Issue Date: 1-Apr-2011
Publisher: Neoplasia Press
Citation: Translational Oncology. Ann Arbor: Neoplasia Press, v. 4, n. 2, p. 101-109, 2011.
Abstract: Melanoma is the most aggressive form of skin cancer, and its incidence has increased dramatically over the years. the murine B16F10 melanoma in syngeneic C57Bl/6 mice has been used as a highly aggressive model to investigate tumor development. Presently, we demonstrate in the B16F10-Nex2 subclone that silencing of SOCS-1, a negative regulator of Jak/Stat pathway, leads to reversal of the tumorigenic phenotype and inhibition of melanoma cell metastasis. SOCS-1 silencing with short hairpin RNA affected tumor growth and cell cycle regulation with arrest at the S phase with large-sized nuclei, reduced cell motility, and decreased melanoma cell invasion through Matrigel. A clonogenic assay showed that SOCS-1 acted as a modulator of resistance to anoikis. in addition, down-regulation of SOCS-1 decreased the expression of epidermal growth factor receptor ( mainly the phosphorylated-R), Ins-R alpha, and fibroblast growth factor receptor. in vivo, silencing of SOCS-1 inhibited subcutaneous tumor growth and metastatic development in the lungs. Because SOCS-1 is expressed in most melanoma cell lines and bears a relation with tumor invasion, thickness, and stage of disease, the present results on the effects of SOCS-1 silencing in melanoma suggest that this regulating protein can be a target of cancer therapy.
URI: http://repositorio.unifesp.br/handle/11600/33578
ISSN: 1936-5233
Other Identifiers: http://dx.doi.org/10.1593/tlo.10250
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