PRMT2 links histone H3R8 asymmetric dimethylation to oncogenic activation and tumorigenesis of glioblastoma

Feng Dong, Qian Li, Chao Yang, Dawei Huo, Xing Wang, Chunbo Ai, Yu Kong, Xiaoyu Sun, Wen Wang, Yan Zhou, Xing Liu, Wei Li, Weiwei Gao, Wen Liu, Chunsheng Kang () and Xudong Wu ()
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Feng Dong: Tianjin Medical University, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics
Qian Li: Tianjin Medical University, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics
Chao Yang: Tianjin Medical University General Hospital
Dawei Huo: Tianjin Medical University, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics
Xing Wang: Tianjin Medical University, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics
Chunbo Ai: Tianjin Medical University, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics
Yu Kong: Tianjin Medical University, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics
Xiaoyu Sun: Tianjin Medical University, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics
Wen Wang: Wuhan University
Yan Zhou: Wuhan University
Xing Liu: Capital Medical University, 6 Tiantanxi Li
Wei Li: Tianjin Nankai Hospital
Weiwei Gao: Xiamen University, Xiamen
Wen Liu: Xiamen University, Xiamen
Chunsheng Kang: Tianjin Medical University General Hospital
Xudong Wu: Tianjin Medical University, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Transcriptional deregulation has a vital role in glioblastoma multiforme (GBM). Thus, identification of epigenetic modifiers essential for oncogenic transcriptional programs is a key to designing effective therapeutics for this deadly disease. Here we report that Protein Arginine Methyltransferase 2 (PRMT2) is highly expressed in GBM and correlated with poor prognosis. The silencing or inactivation of PRMT2 inhibits GBM cell growth and glioblastoma stem cell self-renewal in vitro, and suppresses orthotopic tumor growth, accompanied with significant deregulation of genes mainly associated with cell cycle progression and pathways in cancer. Mechanistically PRMT2 is responsible for H3R8 asymmetric methylation (H3R8me2a), whose enrichment at promoters and enhancers is closely correlated with known active histone marks and is required for the maintenance of target gene expression. Together, this study demonstrates that PRMT2 acts as a transcriptional co-activator for oncogenic gene expression programs in GBM pathogenesis and provides a rationale for PRMT2 targeting in aggressive gliomas.

Date: 2018
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DOI: 10.1038/s41467-018-06968-7

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