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CDC20 maintains tumor initiating cells
Journal article   Open access   Peer reviewed

CDC20 maintains tumor initiating cells

Qi Xie, Qiulian Wu, Stephen C. Mack, Kailin Yang, Leo Kim, Christopher G. Hubert, William A. Flavahan, Chengwei Chu, Shideng Bao and Jeremy N. Rich
Oncotarget, Vol.6(15), pp.13241-13254
05/30/2015
DOI: 10.18632/oncotarget.3676
PMCID: PMC4537011
PMID: 25938542
url
https://doi.org/10.18632/oncotarget.3676View
Published (Version of record) Open Access

Abstract

Glioblastoma is the most prevalent and lethal primary intrinsic brain tumor. Glioblastoma displays hierarchical arrangement with a population of self-renewing and tumorigenic glioma tumor initiating cells (TICs), or cancer stem cells. While non-neoplastic neural stem cells are generally quiescent, glioblastoma TICs are often proliferative with mitotic control offering a potential point of fragility. Here, we interrogate the role of cell-division cycle protein 20 (CDC20), an essential activator of anaphase-promoting complex (APC) E3 ubiquitination ligase, in the maintenance of TICs. By chromatin analysis and immunoblotting, CDC20 was preferentially expressed in TICs relative to matched non-TICs. Targeting CDC20 expression by RNA interference attenuated TIC proliferation, self-renewal and in vivo tumor growth. CDC20 disruption mediated its effects through induction of apoptosis and inhibition of cell cycle progression. CDC20 maintains TICs through degradation of p21(CIP1/WAF1), a critical negative regulator of TICs. Inhibiting CDC20 stabilized p21(CIP1/WAF1), resulting in repression of several genes critical to tumor growth and survival, including CDC25C, c-Myc and Survivin. Transcriptional control of CDC20 is mediated by FOXM1, a central transcription factor in TICs. These results suggest CDC20 is a critical regulator of TIC proliferation and survival, linking two key TIC nodes -FOXM1 and p21(CIP1/WAF1) - elucidating a potential point for therapeutic intervention.
Cell Biology Life Sciences & Biomedicine Oncology Science & Technology

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