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

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.