Carfilzomib enhances cisplatin-induced apoptosis in SK-N-BE(2)-M17 human neuroblastoma cells
- Authors
- Lee, Song-, I; Jeong, Yeon Ju; Yu, Ah-Ran; Kwak, Hyeok Jin; Cha, Ji-Young; Kang, Insug; Yeo, Eui-Ju
- Issue Date
- 25-Mar-2019
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- SCIENTIFIC REPORTS, v.9
- Journal Title
- SCIENTIFIC REPORTS
- Volume
- 9
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/1702
- DOI
- 10.1038/s41598-019-41527-0
- ISSN
- 2045-2322
- Abstract
- Neuroblastoma is a solid malignant tumor of the sympathetic nervous system, which accounts for 8-10% of childhood cancers. Considering the overall high risk and poor prognosis associated with neuroblastoma, effective therapeutics should be developed to improve patient survival and quality of life. A recent study showed that a proteasome inhibitor, carfilzomib (CFZ), reduced cell viability of SK-N-BE(2)-M17 neuroblastoma cells. Therefore, we investigated the molecular mechanisms by which CFZ lower the cell viability of neuroblastoma cells. CFZ reduced cell viability via cell cycle arrest at G2/M and apoptosis, which involved caspase activation (caspases-8, 9, 4, and 3), endoplasmic reticulum stress, reactive oxygen species production, mitochondria! membrane potential loss, and autophagy in a dose and time-dependent manner. The effect of CFZ was additive to that of cisplatin (Cis), a well-known chemotherapeutic drug, in terms of cell viability reduction, cell cycle arrest, and apoptosis. Importantly, the additive effect of CFZ was maintained in Cis-resistant neuroblastoma cells. These results suggest that CFZ can be used in combination therapy for patients with neuroblastoma to overcome the resistance and adverse side effects of Cis.
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