Content area

Abstract

Cancer stem cells (CSCs) play an important role in osteosarcoma (OS) metastasis and recurrence, and both Wnt/β-catenin and Notch signaling are essential for the development of the biological traits of CSCs. However, the mechanism that underlies the simultaneous hyperactivation of both Wnt/β-catenin and Notch signaling in OS remains unclear. Here, we report that expression of miR-135b correlates with the overall and recurrence-free survival of OS patients, and that miR-135b has an activating effect on both Wnt/β-catenin and Notch signaling. The overexpression of miR-135b simultaneously targets multiple negative regulators of the Wnt/β-catenin and Notch signaling pathways, including glycogen synthase kinase-3 beta (GSK3β), casein kinase 1a (CK1α), and ten-eleven translocation 3 (TET3). Therefore, upregulated miR-135b promotes CSC traits, lung metastasis, and tumor recurrence in OS. Notably, antagonizing miR-135b potently inhibits OS lung metastasis, cancer cell stemness, CSC-induced tumor formation, and recurrence in xenograft animal models. These findings suggest that miR-135b mediates the constitutive activation of Wnt/β-catenin and Notch signaling, and that the inhibition of miR-135b is a novel strategy to inhibit tumor metastasis and prevent CSC-induced recurrence in OS.

Details

Title
miR-135b Stimulates Osteosarcoma Recurrence and Lung Metastasis via Notch and Wnt/β-Catenin Signaling
Author
Jin, Hua 1 ; Luo, Song 2 ; Wang, Yun 3 ; Liu, Chang 4 ; Piao, Zhenghao 5 ; Xu, Meng 2 ; Guan, Wei 6 ; Li, Qing 6 ; Zou, Hua 6 ; Tan, Qun-You 6 ; Zhen-Zhou, Yang 6 ; Wang, Yan 2 ; Wang, Dong 6 ; Cheng-Xiong, Xu 6 

 Department of Thoracic Surgery, Daping Hospital and Research Institute of Surgery, Third Military Medical University, Chongqing 400042, China 
 Department of Orthopaedics, The General Hospital of Chinese People’s Liberation Army, Beijing 100853, China 
 Department of Pathology, The General Hospital of Chinese People’s Liberation Army, Beijing 100853, China 
 Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Jilin University, Changchun 130021, China 
 Department of Basic Medical Science, School of Medicine, Hangzhou Normal University, Hangzhou 310036, China 
 Cancer Center, Daping Hospital and Research Institute of Surgery, Third Military Medical University, Chongqing 400042, China 
Pages
111-122
Section
Original Article
Publication year
2017
Publication date
Sep 15, 2017
Publisher
Elsevier Limited
e-ISSN
21622531
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2308415764
Copyright
©2017. The Author(s)