Atractylenolide I-mediated Notch pathway inhibition attenuates gastric cancer stem cell traits

被引：78

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

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2014年 / 450卷 / 01期

关键词：

Gastric cancer; Cancer stem cells; Atractylenolide I; Notch; CD44; ATRACTYLODES-MACROCEPHALA; EXPRESSION; JAPONICA; MARKERS; TUMOR; CD44;

D O I：

10.1016/j.bbrc.2014.05.110

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

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.

引用

页码：353 / 359

页数：7

共 29 条

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