J Cancer 2017; 8(11):2069-2078. doi:10.7150/jca.19143
Opposite Effects of SET7/9 on Apoptosis of Human Acute Myeloid Leukemia Cells and Lung Cancer Cells
1. Department of Pathophysiology, Medical school of Southeast University, Nanjing, Jiangsu, China, 210009.
2. Department of Laboratory Medicine, Cross Cancer Institute, University of Alberta, Edmonton, Alberta, Canada
Gu Y, Wang Y, Wang X, Gao L, Yu W, Dong WF. Opposite Effects of SET7/9 on Apoptosis of Human Acute Myeloid Leukemia Cells and Lung Cancer Cells. J Cancer 2017; 8(11):2069-2078. doi:10.7150/jca.19143. Available from http://www.jcancer.org/v08p2069.htm
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.
Keywords: SET7/9, AML cell, NSCLC cell, apoptosis, p53, E2F1.