A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Role of SOCS-1 Gene on Melanoma Cell Growth and Tumor Development
Tekijät: Scutti JA, Matsuo AL, Pereira FV, Massaoka MH, Figueiredo CR, Moreira DF, Belizário JE, Travassos LR
Julkaisuvuosi: 2011
Lehti:: Translational Oncology
Tietokannassa oleva lehden nimi: Translational oncology
Lehden akronyymi: Transl Oncol
Vuosikerta: 4
Numero: 2
Aloitussivu: 101
Lopetussivu: 9
Sivujen määrä: 9
ISSN: 1936-5233
eISSN: 1936-5233
DOI: https://doi.org/10.1593/tlo.10250
Verkko-osoite: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3069653/pdf/tlo0402_0101.pdf
Rinnakkaistallenteen osoite: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3069653/pdf/tlo0402_0101.pdf
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, downregulation of SOCS-1 decreased the expression of epidermal growth factor receptor (mainly the phosphorylated-R), Ins-Rα, 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.
Ladattava julkaisu This is an electronic reprint of the original article. |  |
