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- Title
IMB-6G induces endoplasmic reticulum stress-mediated apoptosis in human nasopharyngeal carcinoma cells.
- Authors
Pan, Yeting; Zhang, Yanni; Gong, Liang; Zou, Jianding; Hu, Boxia; Zhang, Sicong
- Abstract
IMB-6G is a novel N-substituted sophoridine acid that has been reported to have anticancer effects. The purpose of the present study was to investigate the effect and underlying mechanism of IMB-6G on human nasopharyngeal carcinoma (NPC) cells. The NPC cell line C666-1 was used in the present study and treated with different concentrations of IMB-6G (0, 1, 2 and 5 µM) for 24 h. Subsequently, cell viability was determined using the Cell Counting kit-8 assay and cell apoptosis was analyzed by performing flow cytometry. The expression levels of genes and proteins in the current study were determined using reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Results indicated that IMB-6G dose-dependently inhibited C666-1 cell viability and induced apoptosis. It was also revealed that IMB-6G induced apoptosis via inducing endoplasmic reticulum (ER) stress activation. Notably, IMB-6G administration enhanced the expression levels of Binding immunoglobulin protein and CCAAT-enhancer-binding protein homologous protein in C666-1 cells. Further analysis suggested that IMB-6G treatment activated inositol-requiring enzyme 1α (IRE1α) and PKR-like ER kinase (PERK) signaling pathways in C666-1 cells. In addition, silencing of IRE1α and PERK significantly reversed IMB-6G-induced cell growth inhibition and apoptosis. In conclusion, the present findings indicated that IMB-6G induced ER stress-mediated apoptosis through activating IRE1α and PERK signaling pathways. The present study suggests that IMB-6G may be a promising agent for NPC treatment.
- Subjects
ENDOPLASMIC reticulum; FLOW cytometry; CARRIER proteins; NASOPHARYNX cancer; ANTINEOPLASTIC agents
- Publication
Experimental & Therapeutic Medicine, 2018, Vol 16, Issue 5, p4187
- ISSN
1792-0981
- Publication type
Article
- DOI
10.3892/etm.2018.6724