Alantolactone promotes ER stress-mediated apoptosis by inhibition of TrxR1 in triple-negative breast cancer cell lines and in a mouse model

doi:10.1111/jcmm.14139

科研成果详情

题名	Alantolactone promotes ER stress-mediated apoptosis by inhibition of TrxR1 in triple-negative breast cancer cell lines and in a mouse model
作者	Yin, Changtian 1,2; Dai, Xuanxuan2; Huang, Xiangjie 1; Zhu, Wangyu3; Chen, Xi 1; Zhou, Qiulin1; Wang, Canwei 4; Zhao, Chengguang1; Zou, Peng1; Liang, Guang1; Rajamanickam, Vinothkumar 1; Wang, Ouchen2; Zhang, Xiaohua 2; Cui, Ri1
发表日期	2019-03
发表期刊	JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 影响因子和分区
语种	英语
原始文献类型	Article
关键词	alantolactone ER-stress ROS Triple-negative breast cancer TrxR1
其他关键词	ENDOPLASMIC-RETICULUM STRESS ; HUMAN THIOREDOXIN HOMOLOG ; LEUKEMIA-DERIVED FACTOR ; EXPRESSION ; GROWTH ; GRP78/BIP ; INDUCTION ; SYSTEM ; TARGET
摘要	Triple-negative breast cancer (TNBC) is a subtype of breast cancer with poor clinical outcome and currently no effective targeted therapies are available. Alantolactone (ATL), a sesquiterpene lactone, has been shown to have potential anti-tumour activity against various cancer cells. However, the underlying mechanism and therapeutic effect of ATL in the TNBC are largely unknown. In the present study, we found that ATL suppresses TNBC cell viability by reactive oxygen species (ROS) accumulation and subsequent ROS-dependent endoplasmic reticulum (ER) stress both in vitro and in vivo. Thioredoxin reductase 1 (TrxR1) expression and activity of were significantly up-regulated in the TNBC tissue specimens compare to the normal adjacent tissues. Further analyses showed that ATL inhibits the activity of TrxR1 both in vitro and in vivo in TNBC and knockdown of TrxR1 in TNBC cells sensitized ATL-induced cell apoptosis and ROS increase. These results will provide pre-clinical evidences that ATL could be a potential therapeutic agent against TNBC by promoting ROS-ER stress-mediated apoptosis through partly targeting TrxR1.
资助项目	National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81672305, 81622043, 81372380]
出版者	WILEY
出版地	HOBOKEN
ISSN	1582-1838
EISSN	1582-4934
卷号	23 期号:3 页码:2194-2206
DOI	10.1111/jcmm.14139
页数	13
WOS类目	Cell Biology ; Medicine, Research & Experimental
WOS研究方向	Cell Biology ; Research & Experimental Medicine
WOS记录号	WOS:000458920000050
收录类别	SCIE ; SCOPUS ; PUBMED
URL	查看原文
PubMed ID	30609207
SCOPUSEID	2-s2.0-85059554165
通讯作者地址	[Zhang, Xiaohua]Department of Thyroid and Breast Surgery,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,China
Scopus学科分类	Molecular Medicine;Cell Biology
引用统计	被引频次：19[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/11912
专题	药学院（分析测试中心）附属第一医院其他_附属乐清医院（乐清市人民医院）其他_附属舟山医院（舟山医院）
通讯作者	Zhang, Xiaohua
作者单位	1.Chemical Biology Research Center,School of Pharmaceutical Sciences,Wenzhou Medical University,Wenzhou,China; 2.Department of Thyroid and Breast Surgery,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,China; 3.Cell and Molecular Biology Laboratory,Zhoushan Hospital of Wenzhou Medical University,Zhoushan,China; 4.Affiliated Yueqing Hospital and School of Pharmaceutical Sciences,Wenzhou Medical University,Wenzhou,China
第一作者单位	药学院（分析测试中心）; 生物有机与药物化学研究中心; 附属第一医院; 第一临床医学院（信息与工程学院）、附属第一医院
通讯作者单位	附属第一医院; 第一临床医学院（信息与工程学院）、附属第一医院
第一作者的第一单位	药学院（分析测试中心）
推荐引用方式 GB/T 7714	Yin, Changtian,Dai, Xuanxuan,Huang, Xiangjie,et al. Alantolactone promotes ER stress-mediated apoptosis by inhibition of TrxR1 in triple-negative breast cancer cell lines and in a mouse model[J]. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE,2019,23(3):2194-2206.
APA	Yin, Changtian., Dai, Xuanxuan., Huang, Xiangjie., Zhu, Wangyu., Chen, Xi., ... & Cui, Ri. (2019). Alantolactone promotes ER stress-mediated apoptosis by inhibition of TrxR1 in triple-negative breast cancer cell lines and in a mouse model. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 23(3), 2194-2206.
MLA	Yin, Changtian,et al."Alantolactone promotes ER stress-mediated apoptosis by inhibition of TrxR1 in triple-negative breast cancer cell lines and in a mouse model".JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 23.3(2019):2194-2206.