Journal
ARCHIVES OF TOXICOLOGY
Volume 93, Issue 11, Pages 3367-3383Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00204-019-02579-3
Keywords
Artemisinin; Hepatocellular carcinoma; Hippo-YAP signaling; Mitochondria; Cellular bioenergetics
Categories
Funding
- National Natural Science Foundation of China [31171345, 31570772, 31070710, 31771534]
- Zhejiang Provincial Health Department Medical Support Discipline-Nutrition [11-ZC24]
- Zhejiang Medical and Health Platform Project (Key Talents) [2014RCA014]
- Natural Science Foundation of Zhejiang Province [Y16H030065, Y17C070006]
- Key Discipline of Zhejiang Province in Medical Technology (First Class, Category A)
- National Basic Research Program of China (973 Program) [2013CB531702]
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The primary liver cancer (PLC) is one of the leading causes of cancer-related death worldwide. The predominant form of PLC is hepatocellular carcinoma (HCC), which accounts for about 85% of all PLC. Artemisinin (ART) was clinically used as anti-malarial agents. Recently, it was demonstrated to inhibit cell growth and migration in multiple cancer types. However, the molecular mechanism underlying these anti-cancer activity remains largely unknown. Herein, it is discovered that ART dramatically suppresses HCC cell growth in vitro through arresting cell cycle progression, and represses cell migration and invasion via regulating N-cadherin-Snail-E-cadherin axis. In addition, the disruption of cellular bioenergetics contributed to ART-caused cell growth, migration and invasion inhibition. Moreover, ART (100 mg/kg, intraperitoneally) substantially inhibits HCC xenograft growth in vivo. Importantly, Hippo-YAP signal transduction is remarkably inactivated in HCC cells upon ART administration. Collectively, these data reveal a novel mechanism of ART in regulating HCC cell growth, migration, and invasion, which indicates that ART could be considered as a potential drug for the treatment of HCC.
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