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LncRNA CRNDE is activated by SP1 and promotes osteosarcoma proliferation, invasion, and epithelial‐mesenchymal transition via Wnt/β‐catenin signaling pathway
Author(s) -
Ding Qiuyue,
Mo Fengbo,
Cai Xianyi,
Zhang Wenda,
Wang Jinglong,
Yang Shuhua,
Liu Xianzhe
Publication year - 2020
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29607
Subject(s) - epithelial–mesenchymal transition , cancer research , gene knockdown , wnt signaling pathway , vimentin , oncogene , cell growth , biology , mesenchymal stem cell , cell culture , cell cycle , apoptosis , microbiology and biotechnology , signal transduction , cancer , metastasis , immunology , immunohistochemistry , biochemistry , genetics
Abstract Long noncoding RNAs (lncRNAs) were identified as a vital part in the development and progression of cancer in recent years. Colorectal neoplasia differentially expressed (CRNDE), a lncRNA, functions as an oncogene in some malignant neoplasias, but its role in the progression of osteosarcoma (OS) is still poorly understood. To dissect the difference in the expression of CRNDE, quantitative real‐time polymerase chain reaction was utilized to evaluate it in OS tissues and cell lines (U2OS, MG63, and MNNG/HOS) compared with that in the adjacent normal tissues/osteoblast cells (hFOB1.19). The role of CRNDE in OS lines was assessed using Cell Counting Kit‐8, colony formation, 5‐ethynyl‐2′‐deoxyuridine staining, terminal deoxynucleotidyl transferase‐mediated deoxyuridine triphosphate nick‐end labeling staining, flow cytometry, Transwell assays, and Western blot, respectively. The results demonstrated that the expression of CRNDE was high in OS tissues and cell lines, and partly induced by SP1. CRNDE knockdown attenuated OS cell proliferation and invasion and induced apoptosis and G0/G1 arrest. Moreover, the expression of mesenchymal markers N‐cadherin, Vimentin and Snail were downregulated, while the expression of epithelial markers E‐cadherin and ZO‐1 were conversely upregulated due to CRNDE knockdown. The mechanistic investigations showed that CRNDE promoted glycogen synthase kinase‐3β phosphorylation to activate the Wnt/β‐catenin pathway. The results suggested that lncRNA CRNDE indeed contributed to OS proliferation, invasion, and epithelial‐mesenchymal transition, working as an oncogene, demonstrating that lncRNA CRNDE may be a valid therapeutic target for the OS.