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

State Key Laboratory of Chinese Medicine and Molecular Pharmacology (Incubation), Shenzhen Research Institute, The Hong Kong Polytechnic University, Shenzhen 518057, China
Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hung Hom 999077, Hong Kong, China
Department of Chemistry, The Hong Kong Baptist University, Kowloon Tong 999077, Hong Kong, China
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;
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)
PDF [4362 KB, uploaded 17 May 2019]


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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