Data/hora: 01/06/2024 01:31:55

Provedor de dados: 	56	
País: 	Brazil	
Título: 	A combination of STI571 and BCR-ABL1 siRNA with overexpressed p15INK4B induced enhanced proliferation inhibition and apoptosis in chronic myeloid leukemia	
Autores: 	Xia,D.Y.; Liu,L.; Hao,M.W.; Liu,Q.; Chen,R.A.; Liang,Y.M.	
Data: 	2014-12-01	
Ano: 	2014	
Palavras-chave: 	Apoptosis Chronic myeloid leukemia p15INK4B STI571 (Gleevec; Imatinib).	
Resumo: 	p15INK4B, a cyclin-dependent kinase inhibitor, has been recognized as a tumor suppressor. Loss of or methylation of the p15INK4B gene in chronic myeloid leukemia (CML) cells enhances myeloid progenitor formation from common myeloid progenitors. Therefore, we examined the effects of overexpressed p15INK4B on proliferation and apoptosis of CML cells. Overexpression of p15INK4B inhibited the growth of K562 cells by downregulation of cyclin-dependent kinase 4 (CDK4) and cyclin D1 expression. Overexpression of p15INK4B also induced apoptosis of K562 cells by upregulating Bax expression and downregulating Bcl-2 expression. Overexpression of p15INK4B together with STI571 (imatinib) or BCR-ABL1 small interfering RNA (siRNA) also enhanced growth inhibition and apoptosis induction of K562 cells. The enhanced effect was also mediated by reduction of cyclin D1 and CDK4 and regulation of Bax and Bcl-2. In conclusion, our study may provide new insights into the role of p15INK4B in CML and a potential therapeutic target for overcoming tyrosine kinase inhibitor resistance in CML.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2014001201096	
Editor: 	Associação Brasileira de Divulgação Científica	
Relação: 	10.1590/1414-431X20143734	
Formato: 	text/html	
Fonte: 	Brazilian Journal of Medical and Biological Research  v.47 n.12 2014	
Fonte: 	info:eu-repo/semantics/openAccess