HP1α is highly expressed in glioma cells and facilitates cell proliferation and survival.

Epigenetic alteration plays critical roles in gliomagenesis by regulating gene expression through modifications of Histones and DNA. Trimethylation of H3K9, an essential repressed transcription mark, and one of its methyltransferase, SUV39H1, are implicated in glioma pathogenesis and progression. We find that the protein level of HP1α, a reader of H3K9me3 is elevated in GOS3 and 1321N1 glioma cell lines. H3K9me3 and SUV39H1 level are also upregulated. Depletion of HP1α and SUV39H1 weakens GOS3 and 1321N1 cell proliferation capacity and results in apoptosis of cells. Furthermore, we find that HP1α and H3K9me3 are enriched in the FAS and PUMA promoters, which suggests that upregulated HP1α and H3K9me3 prevent apoptosis by suppressing apoptotic activators. These data indicates that up-regulated HP1α, SUV39H1, and H3K9me3 in glioma cells are functionally associated with glioma pathogenesis and progression, and may serve as novel biomarkers for future diagnostic and therapeutic targeting of brain tumors.