Aberrantly expressed miR-582-3p maintains lung cancer stem cell-like traits by activating Wnt/β-catenin signalling

Lishan Fang, Junchao Cai, Baixue Chen, Shanshan Wu, Rong Li, Xiaonan Xu, Yi Yang, Hongyu Guan, Xun Zhu, Le Zhang, Jie Yuan, Jueheng Wu and Mengfeng Li ()
Additional contact information
Lishan Fang: Sun Yat-sen University
Junchao Cai: Sun Yat-sen University
Baixue Chen: Sun Yat-sen University
Shanshan Wu: Sun Yat-sen University
Rong Li: Sun Yat-sen University
Xiaonan Xu: Sun Yat-sen University
Yi Yang: Key Laboratory of Tropical Disease Control, Sun Yat-sen University, Ministry of Education
Hongyu Guan: The First Affiliated Hospital of Sun Yat-sen University
Xun Zhu: Sun Yat-sen University
Le Zhang: Sun Yat-sen University
Jie Yuan: Key Laboratory of Tropical Disease Control, Sun Yat-sen University, Ministry of Education
Jueheng Wu: Sun Yat-sen University
Mengfeng Li: Sun Yat-sen University

Nature Communications, 2015, vol. 6, issue 1, 1-15

Abstract: Abstract Cancer stem cells (CSCs) are involved in tumorigenesis, tumour recurrence and therapy resistance and Wnt signalling is essential for the development of the biological traits of CSCs. In non-small cell lung carcinoma (NSCLC), unlike in colon cancer, mutations in β-catenin and APC genes are uncommon; thus, the mechanism underlying the constitutive activation of Wnt signalling in NSCLC remains unclear. Here we report that miR-582-3p expression correlates with the overall- and recurrence-free-survival of NSCLC patients, and miR-582-3p has an activating effect on Wnt/β-catenin signalling. miR-582-3p overexpression simultaneously targets multiple negative regulators of the Wnt/β-catenin pathway, namely, AXIN2, DKK3 and SFRP1. Consequently, miR-582-3p promotes CSC traits of NSCLC cells in vitro and tumorigenesis and tumour recurrence in vivo. Antagonizing miR-582-3p potently inhibits tumour initiation and progression in xenografted animal models. These findings suggest that miR-582-3p mediates the constitutive activation of Wnt/β-catenin signalling, likely serving as a potential therapeutic target for NSCLC.

Date: 2015
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms9640 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9640

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms9640

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().