USF1 prompt melanoma through upregulating TGF-ß signaling pathway.
Eur Rev Med Pharmacol Sci
; 20(17): 3592-8, 2016 09.
Article
em En
| MEDLINE
| ID: mdl-27649659
ABSTRACT
OBJECTIVE:
The activation of TGF-ß signaling contributes to abnormal EMT process and upstream stimulatory family1 (USF1) was recently found to activate the expression of TGF-ß. However, the specific role of USF1 in melanoma has never been explored. MATERIALS ANDMETHODS:
The expression of USF1 was analyzed using real-time PCR and Western blot. The changes of cell morphology were observed under a microscope. Cell migration was determined using in vitro scratch test. A specific siRNA was applied to knockdown of USF1.RESULTS:
The mRNA and protein levels of USF1 were significantly enhanced in melanoma cell lines, 1205-Lu, DO4, WM3211, and WM278, compared with normal human melanocytes PIG1. Overexpression of USF1 induced demonstrated an elongated and spindle-shaped morphology in the 1205-Lu cells. Meanwhile, USF1 induced the expression of α-SMA, Vimentin and Fibronectin, while the epithelial marker, E-cadherin (E-cad), was significantly decreased. Furthermore, in vitro scratch test demonstrated that overexpression of USF1 markedly enhanced 1205-Lu cell migration capacity at 24 h and 48 h. More importantly, knockdown of USF1 could partially reverse TGF-ß1-treatment-induced changes of EMT markers as well as cell morphological changes.CONCLUSIONS:
We first demonstrate that overexpression of USF1 prompts the EMT process through the accumulation of TGF-ß1 production in melanoma cells.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Neoplasias Cutâneas
/
Caderinas
/
Fator de Crescimento Transformador beta
/
Fatores Estimuladores Upstream
/
Melanoma
Limite:
Humans
Idioma:
En
Revista:
Eur Rev Med Pharmacol Sci
Assunto da revista:
FARMACOLOGIA
/
TOXICOLOGIA
Ano de publicação:
2016
Tipo de documento:
Article
País de afiliação:
China