详细信息
Atractylenolide I-mediated Notch pathway inhibition attenuates gastric cancer stem cell traits ( SCI-EXPANDED收录)
文献类型:期刊文献
英文题名:Atractylenolide I-mediated Notch pathway inhibition attenuates gastric cancer stem cell traits
作者:Ma, Li[1,2];Mao, Rurong[1,2];Shen, Ke[1,2];Zheng, Yuanhong[1,2];Li, Yueqi[1,2];Liu, Jianwen[1,2];Ni, Lei[3]
机构:[1]E China Univ Sci & Technol, Sch Pharm, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China;[2]E China Univ Sci & Technol, Sch Pharm, Shanghai Key Lab New Drug Design, Shanghai 200237, Peoples R China;[3]Shanghai Jiao Tong Univ, Sch Med, Ruijin Hosp, Dept Respirat, Shanghai 200025, Peoples R China
年份:2014
卷号:450
期号:1
起止页码:353
外文期刊名:BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
收录:;WOS:【SCI-EXPANDED(收录号:WOS:000343641000058)】;
基金:This work was supported by Shanghai Committee of Science and Technology (No. 13140902300), Nano Science and Technology Special Funding of Shanghai Committee of Science and Technology (No. 11nm0503700), the Shanghai Committee of Science and Technology [grant 11DZ2260600] and the Fundamental Research Funds for the Central Universities.
语种:英文
外文关键词:Gastric cancer; Cancer stem cells; Atractylenolide I; Notch; CD44
摘要:Atractylenolide I (AT-I), one of the main naturally occurring compounds of Rhizome Atractylodis Macrocephalae, has remarkable anti-cancer effects on various cancers. However, its effects on the treatment of gastric cancer remain unclear. Via multiple cellular and molecular approaches, we demonstrated that AT-I could potently inhibit cancer cell proliferation and induce apoptosis through inactivating Notch pathway. AT-I treatment led to the reduction of expressions of Notch1, Jagged1, and its downstream Hes1/ Hey1. Our results showed that AT-I inhibited the self-renewal capacity of gastric stem-like cells (GCSLCs) by suppression of their sphere formation capacity and cell viability. AT-I attenuated gastric cancer stem cell (GCSC) traits partly through inactivating Notch1, leading to reducing the expressions of its downstream target Hes1, Hey1 and CD44 in vitro. Collectively, our results suggest that AT-I might develop as a potential therapeutic drug for the treatment of gastric cancer. (C) 2014 Elsevier Inc. All rights reserved.
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