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Molecules 2016, 21(10), 1353; doi:10.3390/molecules21101353

Tetrandrine Induces Apoptosis of Human Nasopharyngeal Carcinoma NPC-TW 076 Cells through Reactive Oxygen Species Accompanied by an Endoplasmic Reticulum Stress Signaling Pathway

1
Department of Biological Science and Technology, China Medical University, Taichung 40402, Taiwan
2
Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung 40402, Taiwan
3
Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung 40402, Taiwan
4
College of Chinese Medicine, School of Post-Baccalaureate Chinese Medicine, China Medical University, Taichung 40402, Taiwan
5
Department of Chinese Medicine, E-Da Hospital, Kaohsiung 82445, Taiwan
6
School of Chinese Medicine for Post-Baccalaureate, I-Shou University, Kaohsiung 82445, Taiwan
7
Department of Health and Nutrition Biotechnology, Asia University, Wufeng, Taichung 41354, Taiwan
8
School of Dentistry, China Medical University, Taichung 40402, Taiwan
9
Department of Biotechnology, Asia University, Wufeng, Taichung 41354, Taiwan
*
Authors to whom correspondence should be addressed.
Academic Editor: Derek J. McPhee
Received: 24 August 2016 / Revised: 7 October 2016 / Accepted: 8 October 2016 / Published: 12 October 2016
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Abstract

Nasopharyngeal carcinoma (NPC) is an epithelial malignancy of the head and neck and the incidence is higher in Southeast Asia. Tetrandrine (TET) is a bisbenzylisoquinoline alkaloid, a natural product, and exhibits biological activities including action against many human cancer cell lines. However, the molecular mechanism of TET-induced cell apoptosis in human NPC cells is still unclear. In the present study, we investigated TET-induced apoptotic cell death and associated possible signal pathways on human nasopharyngeal carcinoma NPC-TW 076 cells in vitro. Phase contrast microscopy was used to examine cell morphology and DAPI staining was used to examine chromatin condensation. Flow cytometry assay was used to measure total viable cells, cell cycle and sub-G1 phase distribution, reactive oxygen species (ROS), Ca2+, and mitochondria membrane potential (ΔΨm) in NPC-TW 076 cells. Results indicate that TET induced cell death through the cell morphological changes, caused G0/G1 phase arrest, increased ROS and Ca2+ production, and finally caused apoptotic cell death in NPC-TW 076 cells. There was no influence on the level of ΔΨm after TET treatment. Western blotting indicated that TET increased endoplasmic reticulum (ER) stress associated protein expression such as GADD153, GRP78, ATF-6α and ATF-6 βwhich indicated that TET induced cell death through ER stress. ER stress is a potential target in cancer treatment, so the ability of TET to induce ER stress response and to activate programming cell death in NPC-TW 076 cells make this molecule become a promising anticancer agent. View Full-Text
Keywords: tetrandrine (TET); endoplasmic reticulum (ER) stress; reactive oxygen species (ROS); apoptosis; NPC-TW 076 cells tetrandrine (TET); endoplasmic reticulum (ER) stress; reactive oxygen species (ROS); apoptosis; NPC-TW 076 cells
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Lin, Y.-J.; Peng, S.-F.; Lin, M.-L.; Kuo, C.-L.; Lu, K.-W.; Liao, C.-L.; Ma, Y.-S.; Chueh, F.-S.; Liu, K.-C.; Yu, F.-S.; Chung, J.-G. Tetrandrine Induces Apoptosis of Human Nasopharyngeal Carcinoma NPC-TW 076 Cells through Reactive Oxygen Species Accompanied by an Endoplasmic Reticulum Stress Signaling Pathway. Molecules 2016, 21, 1353.

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