Circular RNA CDR1as-induced autophagy regulates the proliferation and migration of CD44(+)/CD24(-) phenotype breast cancer stem cells in vitro

doi:10.1080/26895293.2021.1934575

科研成果详情

题名	Circular RNA CDR1as-induced autophagy regulates the proliferation and migration of CD44(+)/CD24(-) phenotype breast cancer stem cells in vitro
作者	Ye, Zhi-qiang1,2; Dong, Xu-bin2; Chen, Han-bin 3; Gu, Dian-na3; Qiu, Zheng-jun 1
发表日期	2021
发表期刊	ALL LIFE 影响因子和分区
语种	英语
原始文献类型	Article
关键词	Circular RNA CDR1as microRNA-7 autophagy breast cancer stem cell competitive endogenous RNA
其他关键词	MICRORNA-7 ; AMPK
摘要	Competitive endogenous RNA (ceRNA) plays a vital role in cancer stem cells. In the present study, we aimed to investigate the role of the circular RNA (circRNA) antisense to the cerebellar degeneration-related protein 1 transcript (CDR1as) during competitive inhibition of microRNA-7 (miR-7) in the regulation of autophagy to modulate the proliferation and migration of breast cancer stem cells. The CD44(+)/CD24(-) phenotype breast cancer stem cells were sorted from the original MCF7 cell by flow cytometry. RT-qPCR was applied to assess the expression of CDR1as and miR-7 in MCF7-Parent and MCF7-Stem cells. The activity of autophagy was evaluated followed the knockdown and overexpression of CDR1as. The correlation between CDR1as and miR-7 and between CDR1as and miR-7-target mRNAs were evaluated. This study revealed that CDR1as overexpression was associated with up-regulation of autophagy and that CDR1as competitive inhibition of miR-7 enhanced the LKB1-AMPK-mTOR signaling and autophagy-associated genes in breast cancer stem cells. CDR1as promoted the cell growth and migration of breast CSCs via the CDR1as/miR-7 axis, and knockdown of CDR1as and miR-7 overexpression obviously impaired the ability of growth and migration. The present study added a new view of developing a new therapeutic strategy against breast cancer.
资助项目	National Natural Science Foundation of ChinaNational Natural Science Foundation of China (NSFC) [81802328]; Wenzhou Science and Technology Plan Project [Y20180846]; Young Talents Program of the First Affiliated Hospital of Wenzhou Medical University [qnyc094]
出版者	TAYLOR & FRANCIS LTD
出版地	ABINGDON
ISSN	2689-5293
EISSN	2689-5307
卷号	14 期号:1 页码:569-576
DOI	10.1080/26895293.2021.1934575
页数	8
WOS类目	Multidisciplinary Sciences
WOS研究方向	Science & Technology - Other Topics
WOS记录号	WOS:000657913800001
收录类别	SCIE ; SCOPUS
URL	查看原文
SCOPUSEID	2-s2.0-85107206070
通讯作者地址	[Qiu, Zheng-jun]Department of Medical Oncology,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,325000,China ; [Gu, Dian-na]Department of Medical Oncology,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,325000,China
Scopus学科分类	Neuroscience (all);Biochemistry, Genetics and Molecular Biology (all);Agricultural and Biological Sciences (all)
引用统计	被引频次：1[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/18035
专题	附属第一医院_肿瘤内科
通讯作者	Gu, Dian-na; Qiu, Zheng-jun
作者单位	1.Department of General surgery,Shanghai General Hospital of Nanjing Medical University,Shanghai,China; 2.Department of Breast Surgery,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,China; 3.Department of Medical Oncology,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,China
第一作者单位	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
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
推荐引用方式 GB/T 7714	Ye, Zhi-qiang,Dong, Xu-bin,Chen, Han-bin,et al. Circular RNA CDR1as-induced autophagy regulates the proliferation and migration of CD44(+)/CD24(-) phenotype breast cancer stem cells in vitro[J]. ALL LIFE,2021,14(1):569-576.
APA	Ye, Zhi-qiang, Dong, Xu-bin, Chen, Han-bin, Gu, Dian-na, & Qiu, Zheng-jun. (2021). Circular RNA CDR1as-induced autophagy regulates the proliferation and migration of CD44(+)/CD24(-) phenotype breast cancer stem cells in vitro. ALL LIFE, 14(1), 569-576.
MLA	Ye, Zhi-qiang,et al."Circular RNA CDR1as-induced autophagy regulates the proliferation and migration of CD44(+)/CD24(-) phenotype breast cancer stem cells in vitro".ALL LIFE 14.1(2021):569-576.