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Artematrolide A inhibited cervical cancer cell proliferation via ROS/ERK/mTOR pathway and metabolic shift
Zhang,Xin-Tian; Hu,Jing; Su,Li-Hua; Geng,Chang-An; Chen,Ji-Jun
2021
Source PublicationPHYTOMEDICINE
ISSN0944-7113
Volume91Pages:153707
AbstractBackground: Artematrolide A (AR-A), a guaianolide dimer isolated from Artemisia atrovirens, demonstrated significant inhibitory effect on three human hepatoma cell lines (HepG2, Huh7 and SMMC7721). The anti-cervical cancer effect and mechanism of this compound have yet to be explored. This study is to reveal the role and mechanisms of artematrolide A on cervical cancer cells, and provide the pharmacological understanding of artematrolide A.Purpose: To investigate the function and possible mechanism of artematrolide A on cervical cancer cells in vitro.Methods: HeLa S3 and SiHa cells were treated with artematrolide A at various concentrations. In this study, MTT, colony formation, cell migration and invasion, cell cycle analysis, cell apoptosis, reactive oxygen species (ROS) detection, western blotting, enzyme activity, and lactate production of artematrolide A were evaluated.Results: Artematrolide A inhibited cell viability, proliferation, migration and invasion in a dose-dependent manner, caused cell cycle arrest in G2/M phase, and induced cell apoptosis via Bcl-2/PARP-1. The mechanism of action of artematrolide A included two aspects: artematrolide A suppressed cell proliferation by activating ROS/ERK/mTOR signaling pathway and promoted glucose metabolism from aerobic glycolysis to mitochondrial respiration by activating pyruvate dehydrogenase complex (PDC) and oxoglutarate dehydrogenase complex (OGDC) via inhibiting the activity of alkaline phosphatases (ALP).Conclusion: Artematrolide A exhibited a significant cytotoxic activity on cervical cancer cells, induced G2/M cell cycle arrest and apoptosis by activating ROS/ERK/mTOR signaling pathway and promoting metabolic shift from aerobic glycolysis to mitochondrial respiration, which suggested artematrolide A might be a potential agent for the treatment of cervical cancer.
KeywordArtemisia atrovirens Cervical cancer ERK pathway Cell metabolism ALKALINE-PHOSPHATASE SIGNALING PATHWAY DIFFERENTIATION APOPTOSIS ERK MECHANISMS
DOI10.1016/j.phymed.2021.153707
WOS IDWOS:000696238900054
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Document Type期刊论文
Identifierhttp://ir.kib.ac.cn/handle/151853/73751
Collection中国科学院昆明植物研究所
Affiliation1.[Zhang, Xin-Tian
2.Hu, Jing
3.Su, Li-Hua
4.Geng, Chang-An
5.Chinese Acad Sci, Kunming Inst Bot, State Key Lab Phytochem & Plant Resources West Ch, Yunnan Key Lab Nat Med Chem, Kunming 650201, Yunnan, Peoples R China
6.[Su, Li-Hua
7.Univ Chinese Acad Sci, Beijing 100049, Peoples R China
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Zhang,Xin-Tian,Hu,Jing,Su,Li-Hua,et al. Artematrolide A inhibited cervical cancer cell proliferation via ROS/ERK/mTOR pathway and metabolic shift[J]. PHYTOMEDICINE,2021,91:153707.
APA Zhang,Xin-Tian,Hu,Jing,Su,Li-Hua,Geng,Chang-An,&Chen,Ji-Jun.(2021).Artematrolide A inhibited cervical cancer cell proliferation via ROS/ERK/mTOR pathway and metabolic shift.PHYTOMEDICINE,91,153707.
MLA Zhang,Xin-Tian,et al."Artematrolide A inhibited cervical cancer cell proliferation via ROS/ERK/mTOR pathway and metabolic shift".PHYTOMEDICINE 91(2021):153707.
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