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 HP1 alpha, a reader of H3K9me3 is elevated in cultured glioma cell lines and glioma tissues. H3K9me3 is also upregulated. Depletion of HP1 alpha and SUV39H1 weakens glioma cell proliferation capacity and results in apoptosis of cells. Furthermore, we find that HP1 alpha and H3K9me3 are enriched in the FAS and PUMA promoters, which suggests that upregulated HP1 alpha and H3K9me3 contribute to cell survival by suppressing apoptotic activators. These data suggests that up-regulated HP1 alpha and H3K9me3 in glioma cells are functionally associated with glioma pathogenesis and progression and may serve as novel biomarkers for diagnostic and therapeutic targeting of brain tumors. (C) 2017 Elsevier Inc. All rights reserved.