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Provedor de dados:  BJMBR
País:  Brazil
Título:  Effects of 5-aza-2′deoxycytidine on RECK gene expression and tumor invasion in salivary adenoid cystic carcinoma
Autores:  Zhou,X.Q.
Huang,S.Y.
Zhang,D.S.
Zhang,S.Z.
Li,W.G.
Chen,Z.W.
Wu,H.W.
Data:  2015-03-01
Ano:  2015
Palavras-chave:  RECK
Salivary adenoid cystic carcinoma
5-aza-2′deoxycytidine
Methylation
Transwell assay
Resumo:  Reversion-inducing cysteine-rich protein with kazal motifs (RECK), a novel tumor suppressor gene that negatively regulates matrix metalloproteinases (MMPs), is expressed in various normal human tissues but downregulated in several types of human tumors. The molecular mechanism for this downregulation and its biological significance in salivary adenoid cystic carcinoma (SACC) are unclear. In the present study, we investigated the effects of a DNA methyltransferase (DNMT) inhibitor, 5-aza-2′deoxycytidine (5-aza-dC), on the methylation status of the RECK gene and tumor invasion in SACC cell lines. Methylation-specific PCR (MSP), Western blot analysis, and quantitative real-time PCR were used to investigate the methylation status of the RECK gene and expression of RECK mRNA and protein in SACC cell lines. The invasive ability of SACC cells was examined by the Transwell migration assay. Promoter methylation was only found in the ACC-M cell line. Treatment of ACC-M cells with 5-aza-dC partially reversed the hypermethylation status of the RECK gene and significantly enhanced the expression of mRNA and protein, and 5-aza-dC significantly suppressed ACC-M cell invasive ability. Our findings showed that 5-aza-dC inhibited cancer cell invasion through the reversal of RECK gene hypermethylation, which might be a promising chemotherapy approach in SACC treatment.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2015000300254
Editor:  Associação Brasileira de Divulgação Científica
Relação:  10.1590/1414-431x20144102
Formato:  text/html
Fonte:  Brazilian Journal of Medical and Biological Research v.48 n.3 2015
Direitos:  info:eu-repo/semantics/openAccess
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