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Article

Capsaicin Induces Autophagy and Apoptosis in Human Nasopharyngeal Carcinoma Cells by Downregulating the PI3K/AKT/mTOR Pathway

1
Department of Otolaryngology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung 83301, Taiwan
2
Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Taoyuan City 33302, Taiwan
3
Kaohsiung Chang Gung Head and Neck Oncology Group, Cancer Center, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 83301, Taiwan
4
Department of Neurosurgery, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 83301, Taiwan
5
Graduate Institute of Medical Science and Innovative Research Center of Medicine, College of Health Sciences, Chang Jung Christian University, Tainan 71101, Taiwan
6
Department of Biological Sciences, National Sun Yat-sen University, Kaohsiung 80424, Taiwan
*
Authors to whom correspondence should be addressed.
Int. J. Mol. Sci. 2017, 18(7), 1343; https://doi.org/10.3390/ijms18071343
Received: 9 May 2017 / Revised: 3 June 2017 / Accepted: 20 June 2017 / Published: 23 June 2017
Capsaicin is a potential chemotherapeutic agent for different human cancers. In Southeast China, nasopharyngeal carcinoma (NPC) has the highest incidence of all cancers, but final treatment outcomes are unsatisfactory. However, there is a lack of information regarding the anticancer activity of capsaicin in NPC cells, and its effects on the signaling transduction pathways related to apoptosis and autophagy remain unclear. In the present study, the precise mechanisms by which capsaicin exerts anti-proliferative effects, cell cycle arrest, autophagy and apoptosis were investigated in NPC-TW01 cells. Exposure to capsaicin inhibited cancer cell growth and increased G1 phase cell cycle arrest. Western blotting and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) were used to measure capsaicin-induced autophagy via involvement of the class III PI3K/Beclin-1/Bcl-2 signaling pathway. Capsaicin induced autophagy by increasing levels of the autophagy markers LC3-II and Atg5, enhancing p62 and Fap-1 degradation and increasing caspase-3 activity to induce apoptosis, suggesting a correlation of blocking the PI3K/Akt/mTOR pathway with the above-mentioned anticancer activities. Taken together, these data confirm that capsaicin inhibited the growth of human NPC cells and induced autophagy, supporting its potential as a therapeutic agent for cancer. View Full-Text
Keywords: capsaicin; autophagy; nasopharyngeal carcinoma; PI3K/AKT/mTOR pathway capsaicin; autophagy; nasopharyngeal carcinoma; PI3K/AKT/mTOR pathway
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MDPI and ACS Style

Lin, Y.-T.; Wang, H.-C.; Hsu, Y.-C.; Cho, C.-L.; Yang, M.-Y.; Chien, C.-Y. Capsaicin Induces Autophagy and Apoptosis in Human Nasopharyngeal Carcinoma Cells by Downregulating the PI3K/AKT/mTOR Pathway. Int. J. Mol. Sci. 2017, 18, 1343. https://doi.org/10.3390/ijms18071343

AMA Style

Lin Y-T, Wang H-C, Hsu Y-C, Cho C-L, Yang M-Y, Chien C-Y. Capsaicin Induces Autophagy and Apoptosis in Human Nasopharyngeal Carcinoma Cells by Downregulating the PI3K/AKT/mTOR Pathway. International Journal of Molecular Sciences. 2017; 18(7):1343. https://doi.org/10.3390/ijms18071343

Chicago/Turabian Style

Lin, Yu-Tsai, Hung-Chen Wang, Yi-Chiang Hsu, Chung-Lung Cho, Ming-Yu Yang, and Chih-Yen Chien. 2017. "Capsaicin Induces Autophagy and Apoptosis in Human Nasopharyngeal Carcinoma Cells by Downregulating the PI3K/AKT/mTOR Pathway" International Journal of Molecular Sciences 18, no. 7: 1343. https://doi.org/10.3390/ijms18071343

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