IMB‑6G induces endoplasmic reticulum stress‑mediated apoptosis in human nasopharyngeal carcinoma cells

Pan,Yeting; Zhang,Yanni; Gong,Liang; Zou,Jianding; Hu,Boxia; Zhang,Sicong

doi:10.3892/etm.2018.6724

IMB‑6G induces endoplasmic reticulum stress‑mediated apoptosis in human nasopharyngeal carcinoma cells

Authors:
- Yeting Pan
- Yanni Zhang
- Liang Gong
- Jianding Zou
- Boxia Hu
- Sicong Zhang
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Affiliations: Department of Otorhinolaryngology, Affiliated Cixi Hospital of Wenzhou Medical College, Cixi, Zhejiang 315300, P.R. China
Published online on: September 11, 2018 https://doi.org/10.3892/etm.2018.6724
Pages: 4187-4192

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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.

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