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Harnessing the Therapeutic Potential of Capsaicin and Its Analogues in Pain and Other Diseases
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Molecules 2016, 21(10), 1406; doi:10.3390/molecules21101406

Capsaicin Suppresses Cell Proliferation, Induces Cell Cycle Arrest and ROS Production in Bladder Cancer Cells through FOXO3a-Mediated Pathways

1
Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China
2
Department of Urology, The Fifth Hospital of Wuhan, Wuhan 430050, China
3
Department of Urology, Jingzhou Central Hospital, Jingzhou 434020, China
4
Department of Endocrinology, The First Affiliated Hospital of Zhejiang University, Hangzhou 310003, China
5
Department of Clinical Oncology, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China
6
Center for Medical Science Research, Zhongnan Hospital of Wuhan University, Wuhan 430071, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: Pin Ju Chueh
Received: 7 September 2016 / Revised: 13 October 2016 / Accepted: 18 October 2016 / Published: 21 October 2016
(This article belongs to the Special Issue Capsaicin)
View Full-Text   |   Download PDF [6916 KB, uploaded 21 October 2016]   |  

Abstract

Capsaicin (CAP), a highly selective agonist for transient receptor potential vanilloid type 1 (TRPV1), has been widely reported to exhibit anti-oxidant, anti-inflammation and anticancer activities. Currently, several therapeutic approaches for bladder cancer (BCa) are available, but accompanied by unfavorable outcomes. Previous studies reported a potential clinical effect of CAP to prevent BCa tumorigenesis. However, its underlying molecular mechanism still remains unknown. Our transcriptome analysis suggested a close link among calcium signaling pathway, cell cycle regulation, ROS metabolism and FOXO signaling pathway in BCa. In this study, several experiments were performed to investigate the effects of CAP on BCa cells (5637 and T24) and NOD/SCID mice. Our results showed that CAP could suppress BCa tumorigenesis by inhibiting its proliferation both in vitro and in vivo. Moreover, CAP induced cell cycle arrest at G0/G1 phase and ROS production. Importantly, our studies revealed a strong increase of FOXO3a after treatment with CAP. Furthermore, we observed no significant alteration of apoptosis by CAP, whereas Catalase and SOD2 were considerably upregulated, which could clear ROS and protect against cell death. Thus, our results suggested that CAP could inhibit viability and tumorigenesis of BCa possibly via FOXO3a-mediated pathways. View Full-Text
Keywords: capsaicin; bladder cancer; cell cycle; ROS; migration; xenograft capsaicin; bladder cancer; cell cycle; ROS; migration; xenograft
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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

Qian, K.; Wang, G.; Cao, R.; Liu, T.; Qian, G.; Guan, X.; Guo, Z.; Xiao, Y.; Wang, X. Capsaicin Suppresses Cell Proliferation, Induces Cell Cycle Arrest and ROS Production in Bladder Cancer Cells through FOXO3a-Mediated Pathways. Molecules 2016, 21, 1406.

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