Your browser doesn't support javascript.
loading
Fluvastatin increases tyrosinase synthesis induced by alpha-melanocyte-stimulating hormone in B16F10 melanoma cells.
Galus, Ryszard; Niderla, Justyna; Sladowski, Dariusz; Sajjad, Emir; Wlodarski, Krzysztof; Józwiak, Jaroslaw.
Afiliação
  • Galus R; Department of Histology and Embryology, Center for Biostructure, Medical University of Warsaw, Chalubinskiego 5, PL 02-004 Warszawa, Poland. rgalus@ib.amwaw.edu.pl
Pharmacol Rep ; 62(1): 164-9, 2010.
Article em En | MEDLINE | ID: mdl-20360626
The aim of this study was to evaluate the effect of fluvastatin on the alpha-melanocyte-stimulating hormone-mediated increase in tyrosinase activity in the melanoma B16F10 cell line and to establish whether Akt and extracellular signal-regulated kinase (Erk) inhibition is involved in tyrosinase synthesis after fluvastatin administration. Fluvastatin modulates alpha-melanocyte-stimulating hormone induced melanogenesis by increasing tyrosinase mRNA production, as shown by real time PCR, or tyrosinase protein synthesis, as presented by western blot technique. The stimulatory effect of fluvastatin on melanogenesis was, in part, induced by modulation of cell proliferation (decreased melanoma cell proliferation in G2/M phase) and possibly decrease of Akt. These findings indicate that fluvastatin increases tyrosinase synthesis induced by alpha-melanocyte-stimulating hormone in B16F10 cells and reveal an unknown effect of statin use: their influence on melanin production.
Assuntos
Buscar no Google
Base de dados: MEDLINE Assunto principal: Melanoma Experimental / Alfa-MSH / Ácidos Graxos Monoinsaturados / Monofenol Mono-Oxigenase / Inibidores de Hidroximetilglutaril-CoA Redutases / Indóis Idioma: En Ano de publicação: 2010 Tipo de documento: Article
Buscar no Google
Base de dados: MEDLINE Assunto principal: Melanoma Experimental / Alfa-MSH / Ácidos Graxos Monoinsaturados / Monofenol Mono-Oxigenase / Inibidores de Hidroximetilglutaril-CoA Redutases / Indóis Idioma: En Ano de publicação: 2010 Tipo de documento: Article