Research Paper Volume 12, Issue 8 pp 6793—6807
LINC00514 drives osteosarcoma progression through sponging microRNA-708 and consequently increases URGCP expression
- 1 Department of Spine Surgery, Shandong Provincial ENT Hospital, Shandong Provincial ENT Hospital Affiliated to Shandong University, Ji’nan 250022, Shandong, China
- 2 Department of Traumatic Orthopedics, Shandong Provincial ENT Hospital, Shandong Provincial ENT Hospital Affiliated to Shandong University, Ji’nan 250022, Shandong, China
- 3 Orthopedic and Soft Tissue Surgery, Shandong Cancer Hospital and Institute, Shandong First Medical University and Shandong Academy of Medical Sciences, Ji’nan 250117, Shandong, China
- 4 Department of Orthopedics, Shandong Provincial Third Hospital, Ji’nan 250031, Shandong, China
received: February 3, 2020 ; accepted: March 17, 2020 ; published: April 23, 2020 ;https://doi.org/10.18632/aging.103043
How to Cite
Copyright © 2020 Yu 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.
Long intergenic nonprotein-coding RNA 00514 (LINC00514) is upregulated in papillary thyroid cancer and contributes to its aggressiveness. In this study, we thoroughly explored the expression profile, specific functions, and relevant molecular mechanism of LINC00514 in osteosarcoma (OS). Herein, LINC00514 was significantly upregulated in OS tissues and cells, and increased LINC00514 expression was closely correlated with tumor size, TNM stage, and distant metastasis. OS patients with high LINC00514 expression had shorter overall survival than those with low LINC00514 expression. LINC00514 interference inhibited OS cell proliferation, colony formation, migration, and invasion in vitro but promoted cell apoptosis and G0/G1 cell cycle arrest. LINC00514 downregulation hindered OS tumor growth in vivo. Mechanistically, LINC00514 functioned as a competing endogenous RNA by directly interacting with microRNA-708-5p (miR-708) and consequently increasing the expression of upregulator of cell proliferation (URGCP). Both miR-708 knockdown and URGCP restoration partially neutralized anticancer activities of LINC00514 silencing in OS cells. LINC00514 increases URGCP expression by acting as a competing endogenous RNA for miR-708, thus exerting oncogenic roles in OS progression. In conclusion, the LINC00514/miR-708/URGCP pathway may be a promising target for drug discovery in the future.