Research Papers:
CBX7 is a glioma prognostic marker and induces G1/S arrest via the silencing of CCNE1
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Abstract
Tianfu Yu1,*, Youzhi Wu2,*, Qi Hu3,*, Junxia Zhang1,*, Er Nie1, Weining Wu1, Xiefeng Wang1, Yingyi Wang1, Ning Liu1
1Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China
2Department of Neurosurgery, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China
3Department of Neurosurgery, First People’s Hospital of Yueyang, Yueyang 414000, China
*These authors contributed equally to this work
Correspondence to:
Ning Liu, email: [email protected]
Keywords: CBX7, epigenetics, cell cycle, glioma
Received: November 16, 2016 Accepted: February 15, 2017 Published: March 01, 2017
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.
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