Inhibition of store‑operated Ca2+ entry counteracts the apoptosis of nasopharyngeal carcinoma cells induced by sodium butyrate

Huang,Wei; Ren,Caiping; Huang,Guoling; Liu,Jie; Liu,Weidong; Wang,Lei; Zhu,Bin; Feng,Xiangling; Shi,Jia; Li,Jinlong; Xia,Xiaomeng; Jia,Wei; Chen,Jiawen; Chen,Yuxiang; Jiang,Xingjun

doi:10.3892/ol.2016.5469

Inhibition of store‑operated Ca2+ entry counteracts the apoptosis of nasopharyngeal carcinoma cells induced by sodium butyrate

Authors:
- Wei Huang
- Caiping Ren
- Guoling Huang
- Jie Liu
- Weidong Liu
- Lei Wang
- Bin Zhu
- Xiangling Feng
- Jia Shi
- Jinlong Li
- Xiaomeng Xia
- Wei Jia
- Jiawen Chen
- Yuxiang Chen
- Xingjun Jiang
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Affiliations: Key Laboratory of Carcinogenesis of the Chinese Ministry of Health and Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Xiangya Hospital, Changsha, Hunan 410008, P.R. China, Department of Gynecology and Obstetrics, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China, School of Pharmaceutical Sciences, Central South University, Changsha, Hunan 410008, P.R. China, Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China
Published online on: December 7, 2016 https://doi.org/10.3892/ol.2016.5469
Pages: 921-929

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Abstract

Sodium butyrate (NaBu), a histone deacetylase inhibitor, has demonstrated anti‑tumor effects in several cancers, and is a promising candidate chemotherapeutic agent. However, its roles in nasopharyngeal carcinoma (NPC), an endemic malignant disease in Southern China and Southeast Asia, has rarely been studied. In the present study, MTT assay, colony formation assay, flow cytometry analysis and western blotting were performed to explore the influence of NaBu on NPC cells and its underlying mechanism. NaBu induced morphological changes and inhibited proliferation in 5‑8F and 6‑10B cells. MTT assay revealed that NaBu was cytotoxic to 5‑8F and 6‑10B cells in a dose‑ and time‑dependent manner. Furthermore, flow cytometry analysis revealed that NaBu induced obvious cell apoptosis in 5‑8F and 6‑10B cells due to the activation of the mitochondrial apoptosis axis. In addition, flow cytometry analysis and western blotting demonstrated that NaBu could enhance the Ca2+ influx by promoting store‑operated Ca2+ entry (SOCE) in 5‑8F and 6‑10B cells. Inhibition of SOCE by specific inhibitors or downregulated expression of calcium release‑activated calcium channel protein 1 and stromal interaction molecule 1 could counteract the apoptosis of NPC cells induced by NaBu. Thus, the current study revealed that enhanced SOCE and activated mitochondrial apoptosis axis may account for the mechanisms of cytotoxicity of NaBu in NPC cells, and that NaBu serves as a promising chemotherapeutic agent in NPC therapy.

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