›› 2018, Vol. 38 ›› Issue (1): 1-.doi: 10.3969/j.issn.1674-8115.2018.01.001

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Histone modification and glioma tumorigenesis

Although epigenetic regulation of histone modification has attracted more and more attention, the underlying mechanisms are still unclear. The present review introduces the role of acetylated H3 lysine 23 (H3K23ac) in glioma tumorigenesis, and demonstrates a new mechanism by which H3K23ac regulates gliomagenesis, which may provide novel approaches to glioma treatment.   

  1. Renji-Med X Clinical Stem Cell Research Center, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China
  • Online:2018-01-28 Published:2018-03-09
  • Supported by:
    National Natural Science Foundation of China, 81372704, 81572467; Program for Professor of Special Appointment (Eastern Scholar) at Shanghai Institutions of Higher Learning, 2014024; Shanghai Municipal Education Commission-Gaofeng Clinical Medicine Grant Support, 20161310; New Hundred Talent Program (Outstanding Academic Leader) at Shanghai Municipal Health Bureau, 2017BR021

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Abstract: Although epigenetic regulation of histone modification has attracted more and more attention, the underlying mechanisms are still unclear. The
present review introduces the role of acetylated H3 lysine 23 (H3K23ac) in glioma tumorigenesis, and demonstrates a new mechanism by which H3K23ac
regulates gliomagenesis, which may provide novel approaches to glioma treatment.

Key words: histone modification, glioma, acetylation