Down-regulation of CHERP inhibits neuroblastoma cell proliferation and induces apoptosis through ER stress induction
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Dunke Zhang1,2, Feng Wang1, Yi Pang1, Xiao-xue Ke1, Shunqin Zhu1, Erhu Zhao1, Kui Zhang1, Lixue Chen2 and Hongjuan Cui1
1State Key Laboratory of Silkworm Genome Biology, The Institute of Sericulture and Systems Biology, Southwest University, Chongqing, China
2Laboratory Research Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
Keywords: CHERP, cell proliferation, colony formation, neuroblastoma
Abbreviations: CHERP, calcium homeostasis endoplasmic reticulum protein; ERS, ER stress; Dox, doxorubicin; mTOR, mammalian target of rapamycin; 4E-BP1, eukaryotic initiation factor 4E-binding protein-1.
Received: April 18, 2017 Accepted: August 04, 2017 Published: September 15, 2017
Neuroblastoma is a childhood tumor that is derived from the sympathetic nervous system. In recent years, great progress has been made in our understanding of neuroblastoma. However, applying theories to improve disease outcomes remains challenging. In this study, we observed that calcium homeostasis endoplasmic reticulum protein (CHERP) was involved in the maintenance of neuroblastoma cell proliferation and tumorigenicity. Moreover, elevated CHERP expression was positively correlated with poor patient survival, whereas low CHERP expression was predictive of better outcomes. Additional functional studies showed that CHERP knockdown inhibited neuroblastoma cell proliferation in vitro and resulted in defective tumorigenicity in vivo. Moreover, CHERP depletion suppressed neuroblastoma cell proliferation by inducing endoplasmic reticulum stress and cell apoptosis. Considering the functional roles of CHERP in neuroblastoma development and maintenance, CHERP might function as a novel therapeutic target for neuroblastoma patients.
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