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Down-regulation of CHERP inhibits neuroblastoma cell proliferation and induces apoptosis through ER stress induction.

ABSTRACT: 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.

SUBMITTER: Zhang D

PROVIDER: S-EPMC5655253 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature

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Down-regulation of CHERP inhibits neuroblastoma cell proliferation and induces apoptosis through ER stress induction.

Zhang Dunke D Wang Feng F Pang Yi Y Ke Xiao-Xue XX Zhu Shunqin S Zhao Erhu E Zhang Kui K Chen Lixue L Cui Hongjuan H

Oncotarget 20170915 46

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 p ...[more]

PMID: 29113358

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Project description:Despite the success of imatinib and other tyrosine kinase inhibitors (TKIs), chronic myeloid leukemia (CML) remains largely incurable, and a number of CML patients die due to Abl mutation-related drug resistance and blast crisis. The aim of this study was to evaluate proliferation inhibition and apoptosis induction by down-regulating PPP2R5C gene expression in the imatinib-sensitive and imatinib-resistant CML cell lines K562, K562R (imatinib resistant without an Abl gene mutation), 32D-Bcr-Abl WT (imatinib-sensitive murine CML cell line with a wild type Abl gene) and 32D-Bcr-Abl T315I (imatinib resistant with a T315I Abl gene mutation) and primary cells from CML patients by RNA interference. PPP2R5C siRNAs numbered 799 and 991 were obtained by chemosynthesis. Non-silencing siRNA scrambled control (SC)-treated, mock-transfected, and untreated cells were used as controls. The PPP2R5C mRNA and protein expression levels in treated CML cells were analyzed by quantitative real-time PCR and Western blotting, and in vitro cell proliferation was assayed with the cell counting kit-8 method. The morphology and percentage of apoptosis were revealed by Hoechst 33258 staining and flow cytometry (FCM). The results demonstrated that both siRNAs had the best silencing results after nucleofection in all four cell lines and primary cells. A reduction in PPP2R5C mRNA and protein levels was observed in the treated cells. The proliferation rate of the PPP2R5C-siRNA-treated CML cell lines was significantly decreased at 72 h, and apoptosis was significantly increased. Significantly higher proliferation inhibition and apoptosis induction were found in K562R cells treated with PPP2R5C-siRNA799 than K562 cells. In conclusion, the suppression of PPP2R5C by RNA interference could inhibit proliferation and effectively induce apoptosis in CML cells that were either imatinib sensitive or resistant. Down-regulating PPP2R5C gene expression might be considered as a new therapeutic target strategy for CML, particularly for imatinib-resistant CML.

Dataset Information

Down-regulation of CHERP inhibits neuroblastoma cell proliferation and induces apoptosis through ER stress induction.

Publications

Down-regulation of CHERP inhibits neuroblastoma cell proliferation and induces apoptosis through ER stress induction.

Similar Datasets

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