Epigenetic alterations such as histone modifications and DNA methylation broadly participate in biological functions and gene regulation, and are essential mechanisms in cancer development apart from genetic abnormalities [21, 22]. PcG proteins act as epigenetic regulators of gene expression and play pivotal roles in both physiological and pathological cellular activities [23–32]. CBX7 participates in the interaction between PRC2 and PRC1; another two PcG elements, EZH2 and BMI-1 belonging to PRC2 and PRC1, respectively, are described as oncoproteins [33–35]. However, the role of CBX7 in malignancy is still inconclusive. Our bioinformatics analysis has revealed that CBX7 is strongly linked to control of cell division. Indeed, CBX7 has been shown to repress Ink4a/Arf locus and impair p14Arf/p53- and p16Ink4a/Rb-dependent pathways in prostate cancer, human follicular lymphomas and gastric cancer [1, 2, 4, 36]. However, Ink4a/Arf locuses in U251, U87, and LN229 cells undergo homozygous deletion and the expression of p16Ink4a in HGG is abrogated . This phenomenon partially impair the oncogenic effect of CBX7. Thus CBX7 may possesse dual functions in cell cycle regulation and maintain a balance between cell division and quiescence. We tested p16 levels in three types of patient-derived primary GBM cells (G1, G2 and G3) and one p16-positive cell type (G1) was found (Supplementary Figure 3A). Compared to NHA, the CBX7 level in G1 was similar but G1 had a higher level of cyclin E1 and a lower level of p16 (Supplementary Figure 3A). After the upregulation of CBX7, the p16 expression was decreased and the cyclin E1 level was impaired (Supplementary Figure 3B). Interestingly, cyclin E1 abundance showed no significant difference in siRNA or lentivirus vector transfected NHA cells. By contrast, p16 protein levels were obvious changed along with the alteration of CBX7 in NHA (Supplementary Figure 3B). We suspect that the expression of CCNE1 in normal cells such as NHAs has been fully inhibited so that the regulation CBX7 cannot further effect CCNE1 expression. In cancer cells, cyclin E1 levels are up-regulated and, conversely, p16 levels was limited via various ways so that CBX7 acts as a tumor repressor in part of GBM cells. We assumed that this balance favors cell quiescence, owing to the anomalous genetic characteristics in GBM. To address this issue, we tested the function of CBX7 in glioma in vitro and in vivo.