Data/hora: 04/06/2024 05:33:36

Provedor de dados: 	48	
País: 	Chile	
Título: 	miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting Sirt1	
Autores: 	Zhang,Xia; Li,Yuehua; Wang,Dan; Wei,Xiaoer.	
Data: 	2017-01-01	
Ano: 	2017	
Palavras-chave: 	MiR-22; Tumorigenesis; Radiosensitivity; Breast cancer; Sirt1.	
Resumo: 	Abstract  Background  miR-22 has been shown to be frequently downregulated and act as a tumor suppressor in multiple cancers including breast cancers. However, the role of miR-22 in regulating the radioresistance of breast cancer cells, as well as its underlying mechanism is still not well understood.  Methods  The expressions of miR-22 and sirt1 at mRNA and protein levels were examined by qRT-PCR and Western Blot. The effects of miR-22 overexpression and sirt1 knockdown on cell viability, apoptosis, radiosensitivity, &amp;#947;-H2AX foci formation were evaluated by CCK-8 assay, flow cytometry, colony formation assay, and &amp;#947;-H2AX foci formation assay, respectively. Luciferase reporter assay and qRT-PCR analysis were performed to confirm the interaction between miR-22 and sirt1.  Results  miR-22 was downregulated and sirt1 was upregulated at both mRNA and protein levels in breast cancer cells. miR-22 overexpression or sirt1 knockdown significantly suppressed viability, induced apoptosis, reduced survival fraction, and increased the number of &amp;#947;-H2AX foci in breast cancer cells. Sirt1 was identified as a target of miR-22 and miR-22 negatively regulated sirt1 expression. Ectopic expression of sirt1 dramatically reversed the inhibitory effect of miR-22 on cell viability and promotive effect on apoptotic rates and radiosensitivity in breast cancer cells.  Conclusions  miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting sirt1, providing a promising therapeutic target for breast cancer.	
Tipo: 	Journal article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602017000100220	
Editor: 	Sociedad de Biología de Chile	
Formato: 	text/html	
Fonte: 	Biological Research  v.50 2017