Table 1.

List of other epigenetic-related factors in GSC studies.

Modulator	Epigenetic action	Role and mechanisms
Helicase, lymphocyte-specific HELLS	Member of the ATP-dependent chromatin remodeling SWI2/SNF2 complexes	Maintenance of proliferation and self-renewal of GSCs through binding to the promoters of cell cycle genes, including E2F3 and MYC targets (58).
Lysine-specific demethylase KDM1A/LSD1	Demethylation of mono- and di-methylated lysines 4 and 9 of histone H3	Cell viability, oncosphere formation and tumorigenesis of intracranial xenografts. Rescue by novel inhibitors (59).
Lysine demethylase with Jumonji domain KDM6B/JMJD3	Demethylation of mono- and di-methylated lysine 27 of histone H3	Cell growth and tumorigenesis of intracranial xenografts of pediatric brainstem GSCs. Rescue by treatment with GSKJ4 (60)
Lysine methyltransferase KMT2A/MLL1	Methylation of lysine 4 of histone H3	Upregulation in GSC and in hypoxic GB. GSC growth and self-renewal (61).
Ten–Eleven Translocation TET3	Conversion of 5 mC to 5 hmC	Inhibition of self-renewal and tumorigenesis after downregulation of its repressor, the nuclear receptor NR2E1/TLX (62). In highly aggressive GSCs, maintenance of laminin-integrin α6 signaling pathway-dependent cell survival through TET3 interaction with STAT3 at methylated loci, leading to global increase of 5hmC levels and the upregulation of oncogenes (e.g., c-Myc, surviving, BCL2-like protein BCL-XL (63) ( Figure 1C ). Inhibition of the differentiation marker GFAP (22) after TET3 translocation into the GSC nucleus.
Tripartite motif-containing protein TRIM24	Reader of histone H3 with unmethylated K4 and acetylated K23	Association with tumor grade and GB recurrence (64). In EGFRvIII-expressing glioma cells, association with increased H3K23ac and recruitment of STAT3 to promote GSC proliferation and oncosphere formation ( Figure 1D ). Rescue by treatment with EGFR inhibitor erlotinib (65).