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Arnicolide D, from the herb Centipeda minima, Is a Therapeutic Candidate against Nasopharyngeal Carcinoma

1
State Key Laboratory of Chinese Medicine and Molecular Pharmacology (Incubation), Shenzhen Research Institute, The Hong Kong Polytechnic University, Shenzhen 518057, China
2
Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hung Hom 999077, Hong Kong, China
3
Department of Chemistry, The Hong Kong Baptist University, Kowloon Tong 999077, Hong Kong, China
4
Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100193, China
*
Authors to whom correspondence should be addressed.
Academic Editor: Zhe-Sheng (Jason) Chen
Molecules 2019, 24(10), 1908; https://doi.org/10.3390/molecules24101908
Received: 1 April 2019 / Revised: 29 April 2019 / Accepted: 10 May 2019 / Published: 17 May 2019
(This article belongs to the Collection Natural Products: Anticancer Potential and Beyond)
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Abstract

Nasopharyngeal carcinoma (NPC) is a high morbidity and mortality cancer with an obvious racial and geographic bias, particularly endemic to Southeast China. Our previous studies demonstrated that Centipeda minima extract (CME) exhibited anti-cancer effects in human NPC cell lines. Arnicolide C and arnicolide D are sesquiterpene lactones isolated from Centipeda minima. In this study, for the first time, we investigated their anti-NPC effects and further explored the related molecular mechanisms. The effects of both arnicolide C and arnicolide D were tested in NPC cells CNE-1, CNE-2, SUNE-1, HONE1, and C666-1. The results showed that the two compounds inhibited NPC cell viability in a concentration- and time-dependent manner. As the inhibitory effect of arnicolide D was the more pronounced of the two, our following studies focused on this compound. Arnicolide D could induce cell cycle arrest at G2/M, and induce cell apoptosis. The molecular mechanism of cell cycle regulation and apoptosis induction was investigated, and the results showed that arnicolide D could downregulate cyclin D3, cdc2, p-PI3K, p-AKT, p-mTOR, and p-STAT3, and upregulate cleaved PARP, cleaved caspase 9, and Bax. Regulation of cyclin B1, cdk6, and Bcl-2 expression by arnicolide D showed dynamic changes according to dose and time. Taken together, arnicolide D modulated the cell cycle, activated the caspase signaling pathway, and inhibited the PI3K/AKT/mTOR and STAT3 signaling pathways. These findings provide a solid base of evidence for arnicolide D as a lead compound for further development, and act as proof for the viability of drug development from traditional Chinese medicines. View Full-Text
Keywords: arnicolide D; NPC; anti-proliferation; cell cycle arrest; apoptosis induction arnicolide D; NPC; anti-proliferation; cell cycle arrest; apoptosis induction
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Liu, R.; Dow Chan, B.; Mok, D. .-W.; Lee, C.-S.; Tai, W. .-S.; Chen, S. Arnicolide D, from the herb Centipeda minima, Is a Therapeutic Candidate against Nasopharyngeal Carcinoma. Molecules 2019, 24, 1908.

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