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Opposite Effects of SET7/9 on Apoptosis of Human Acute Myeloid Leukemia Cells and Lung Cancer Cells.
Gu, Ye; Wang, Yuan; Wang, Xinling; Gao, Lili; Yu, Weiping; Dong, Wei-Feng.
Afiliação
  • Gu Y; Department of Pathophysiology, Medical school of Southeast University, Nanjing, Jiangsu, China, 210009.
  • Wang Y; Department of Pathophysiology, Medical school of Southeast University, Nanjing, Jiangsu, China, 210009.
  • Wang X; Department of Pathophysiology, Medical school of Southeast University, Nanjing, Jiangsu, China, 210009.
  • Gao L; Department of Pathophysiology, Medical school of Southeast University, Nanjing, Jiangsu, China, 210009.
  • Yu W; Department of Pathophysiology, Medical school of Southeast University, Nanjing, Jiangsu, China, 210009.
  • Dong WF; Department of Laboratory Medicine, Cross Cancer Institute, University of Alberta, Edmonton, Alberta, Canada.
J Cancer ; 8(11): 2069-2078, 2017.
Article em En | MEDLINE | ID: mdl-28819408
SET7/9 is a protein lysine methyltransferases (PLMTs or PKMTs) which methylates both histone H3K4 and non-histone proteins including transcriptional factors, tumor suppressors, and membrane-associated receptors. Methylation of these proteins alters protein activity and leads to changes in cellular behavior and a series of biological processes. This study aims to investigate the role of SET7/9 in human acute myeloid leukemia (AML) and non-small-cell lung cancer (NSCLC). We examined the expression of SET7/9 in AML cells and NSCLC cells and detected the methylation status of the SET7/9 promoter region. To evaluate the effect of SET7/9 expression changes on cell apoptosis, cell apoptosis rates were determined after SET7/9 overexpression or down-regulation. Our results showed that SET7/9 induces apoptosis of AML cells and inhibits apoptosis of NSCLC cells, suggesting differential effects of SET7/9 on cellular apoptosis and carcinogenesis depending on different cancer types and genetic contexts. Furthermore, we also demonstrated that SET7/9 suppresses cell apoptosis via modulation of E2F1 under circumstance of p53 deficiency in NSCLC cells.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: J Cancer Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: J Cancer Ano de publicação: 2017 Tipo de documento: Article