Abstract
Chromobox homolog 7 (CBX7) cooperates with other polycomb group (PcG) proteins to maintain target genes in a silenced state. However, the precise role of CBX7 in tumor progression is still controversial. We found that the expression of CBX7 in four public databases was significantly lower in high grade glioma (HGG). The reduced expression of CBX7 correlated with poor outcome in HGG patients. Both KEGG and GO analyses indicated that genes that were negatively correlated to CBX7 were strongly associated with the cell cycle pathway. We observed that decreased CBX7 protein levels enhanced glioma cells proliferation, migration and invasion. Then, we verified that CBX7 overexpression arrested cells in the G0/G1 phase. Moreover, we demonstrated that the underlying mechanism involved in CBX7 induced repression of CCNE1 promoter requiring the recruitment of histone deacetylase 2 (HADC2). Finally, in vivo bioluminescence imaging and survival times of nude mice revealed that CBX7 behaved as a tumor suppressor in gliomas. In summary, our results validate the assumption that CBX7 is a tumor suppressor of gliomas. Moreover, CBX7 is a potential and novel prognostic biomarker in glioma patients. We also clarified that CBX7 silences CCNE1 via the combination of CCNE1 promoter and the recruitment of HDAC2.
Highlights
Chromobox homolog 7 (CBX7) is a chromobox family protein which belongs to polycomb repressive complex 1 (PRC1)
Decreased CBX7 expression correlates with glioma grade and its overexpression confers a better prognosis in high grade glioma (HGG) patients
We found that CBX7 mRNA levels in high-grade gliomas (HGG) were significantly decreased compared to normal brain tissues (NBT) and lowgrade gliomas (LGG)
Summary
Chromobox homolog 7 (CBX7) is a chromobox family protein which belongs to polycomb repressive complex 1 (PRC1). In cooperation with other polycomb group (PcG) proteins, CBX7 maintain target genes, which participate in stem cell self-renewal and developmental regulation, in a silenced state [1,2,3,4]. CBX7 recognizes H3K27me, which is catalyzed by enhancer of zeste homolog 2 (EZH2). CBX7 recruits other PRC1 proteins to the target chromatin marked by H3K27me and represses gene transcription [5,6,7]. Besides the PRC-dependent mechanism, recent studies found that CBX7 epigenetically regulates gene expression via the interaction with histone deacetylase 2 (HADC2). The precise role of CBX7 in tumorigenesis and tumor progression is still controversial
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
