Abstract |
Dihydroartemisinin (DHA) has recently been shown anti- tumor activity in various cancer cells. However, its effect on esophageal cancer remains unclear. In this study, for the first time, we demonstrated that DHA reduced viability of esophageal cancer cells in a dose-dependent manner. The mechanism was at least partially due to DHA induced apoptosis by upregulating the expression of Bax, downregulating Bcl-2, Bcl-xL and Procaspase-3, and increasing caspase-9 activation, induced cell cycle arrest by downregulating cyclin E, CDK2 and CDK4. Furthermore, we firstly found that DHA induced autophagy in cancer cells. We concluded DHA might be a novel agent against esophageal cancer.
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Authors | Xiao-Xue Du, Yan-Jing Li, Chun-Long Wu, Jian-Hua Zhou, Yu Han, Hong Sui, Xiao-Li Wei, Lei Liu, Peng Huang, Heng-Heng Yuan, Ting-Ting Zhang, Wen-Jie Zhang, Rui Xie, Xiao-Hui Lang, De-Xin Jia, Yu-Xian Bai |
Journal | Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
(Biomed Pharmacother)
Vol. 67
Issue 5
Pg. 417-24
(Jun 2013)
ISSN: 1950-6007 [Electronic] France |
PMID | 23582790
(Publication Type: Journal Article)
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Copyright | Copyright © 2013 Elsevier Masson SAS. All rights reserved. |
Chemical References |
- Antineoplastic Agents
- Artemisinins
- artenimol
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Topics |
- Antineoplastic Agents
(pharmacology)
- Apoptosis
(drug effects)
- Artemisinins
(administration & dosage, pharmacology)
- Autophagy
(drug effects)
- Cell Cycle Checkpoints
(drug effects)
- Cell Line, Tumor
- Dose-Response Relationship, Drug
- Down-Regulation
(drug effects)
- Esophageal Neoplasms
(drug therapy, pathology)
- Humans
- Up-Regulation
(drug effects)
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