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Research Paper|Volume 12, Issue 7|pp 6172—6190

USF1-mediated upregulation of lncRNA GAS6-AS2 facilitates osteosarcoma progression through miR-934/BCAT1 axis

Guojun Wei1, Tianwei Zhang2, Zongguang Li1, Naichun Yu1, Xiang Xue1, Daguo Zhou1, Yongjie Chen1, Linlin Zhang1, Xiaoli Yao3, Guangrong Ji1
  • 1Department of Orthopaedics, The Xiang’an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361101, Fujian, China
  • 2Department of Anesthesiology, The First Affiliated Hospital of Xiamen University, Xiamen 361003, Fujian, China
  • 3Department of Gastroenterology, The Xiang’an Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361101, Fujian, China
* Equal contribution
Received: October 2, 2019Accepted: February 22, 2020Published: April 8, 2020
https://doi.org/10.18632/aging.103015

Copyright © 2020 Wei et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Long noncoding RNAs (lncRNAs) have been certified as important regulators in tumorigenesis. LncRNA GAS6-AS2 (GAS6-AS2) was a newly identified tumor-related lncRNA, and its dysregulation and oncogenic effects in melanoma and bladder cancer had been reported in previous studies. However, the expression pattern and potential function of GAS6-AS2 in osteosarcoma (OS) have not been investigated. In this study, we identified a novel OS-related lncRNA GAS6-AS2. We found that GAS6-AS2 was distinctly upregulated in both OS specimens and cell lines. Distinct up-regulation of GAS6-AS2 in OS was correlated with advanced clinical stages and shorter survivals. In addition, USF1 could directly bind to the GAS6-AS2 promoter and contribute to its overexpression. Furthermore, GAS6-AS2 knockdown caused tumor suppressive effects via reducing cellular proliferation, migration and invasion, and promoting OS cell apoptosis. Besides, GAS6-AS2 directly bound to miR-934 and downregulated its expression. Mechanistically, GAS6-AS2 positively regulated the expression of BCAT1 through sponging miR-934. Taken together, our data illustrated how GAS6-AS2 played an oncogenic role in OS and might offer a potential therapeutic target for treating OS.