J Cancer 2017; 8(11):2069-2078. doi:10.7150/jca.19143

Research Paper

Opposite Effects of SET7/9 on Apoptosis of Human Acute Myeloid Leukemia Cells and Lung Cancer Cells

Ye Gu1, Yuan Wang1, Xinling Wang1, Lili Gao1, Weiping Yu1✉, Wei-Feng Dong2✉

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

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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

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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.