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Effect of Meisoindigo on Wnt signal pathway in K562 and HL-60 cells / 中国实验血液学杂志
Article em Zh | WPRIM | ID: wpr-243309
Biblioteca responsável: WPRO
ABSTRACT
The aim of this study was to investigate the effect of meisoindigo on Wnt signal pathway in K562 cells and HL-60 cells and its possible regulatory mechanism. RT-PCR and Western blot assay were used to detect the expression of GSK-3beta and its downstream associated genes as well as proteins expression respectively. The results showed that the meisoindigo could inhibit the phosphorylation of GSK-3beta and decreased beta-catenin and c-myc genes expression in HL-60 cells, but did not significantly affect the two gene expression in K562 cells. Meisoindigo slightly increased the expression of GSK-3beta protein in HL-60 cells, obviously decreased the expression of p-GSK-3beta and c-MYC proteins in K562 cells and HL-60 cells, while meisoindigo did not affect the expression of beta-catenin in K562 cells significantly, but could decrease the expression of beta-catenin in HL-60 cells. It is concluded that the meisoindigo can affect the Wnt signal pathway through inhibiting the GSK-3beta expression and down-regulating the beta-catenin and c-MYC protein expression, which play an important role in the treatment for chronic myeloid leukemia.
Assuntos
Texto completo: 1 Índice: WPRIM Assunto principal: Farmacologia / Transdução de Sinais / Proteínas Proto-Oncogênicas c-myc / Células HL-60 / Células K562 / Quinase 3 da Glicogênio Sintase / Proteínas Wnt / Beta Catenina / Glicogênio Sintase Quinase 3 beta / Indóis Limite: Humans Idioma: Zh Revista: Journal of Experimental Hematology Ano de publicação: 2010 Tipo de documento: Article
Texto completo: 1 Índice: WPRIM Assunto principal: Farmacologia / Transdução de Sinais / Proteínas Proto-Oncogênicas c-myc / Células HL-60 / Células K562 / Quinase 3 da Glicogênio Sintase / Proteínas Wnt / Beta Catenina / Glicogênio Sintase Quinase 3 beta / Indóis Limite: Humans Idioma: Zh Revista: Journal of Experimental Hematology Ano de publicação: 2010 Tipo de documento: Article