Research Paper Volume 13, Issue 4 pp 6091—6102
Circ_0000527 promotes osteosarcoma cell progression through modulating miR-646/ARL2 axis
- 1 Department of Orthopaedic Surgery, Nanyang Second People's Hospital, Nanyang 473000, Henan, China
- 2 Department of Medical Oncology, Nanyang Second People's Hospital, Nanyang 473000, Henan, China
Received: July 23, 2020 Accepted: November 25, 2020 Published: February 22, 2021https://doi.org/10.18632/aging.202602
How to Cite
Copyright: © 2021 Wu 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.
Accumulating evidence shows that circRNAs play critical roles in the development of human tumors. We observed that circ_0000527 was overexpressed in osteosarcoma cells (SAOS-2, HOS, MG-63 and U2OS) compared in hFOB1.19 cells. We demonstrated that the circ_0000527 level was higher in osteosarcoma specimens than in non-tumor specimens. The ectopic expression of circ_0000527 was shown to induce cell growth, cell cycle progression and the secretion of inflammatory mediators, including IL-1β, IL-6, IL-8 and TNF-α. We demonstrated that circ_0000527 sponges miR-646 in osteosarcoma cells and that ARL2 is a target gene of miR-646. MiR-646 expression was decreased and ARL2 was overexpressed in osteosarcoma cells (SAOS-2, HOS, MG-63 and U2OS) compared to hFOB1.19 cells. Overexpression of circ_0000527 was demonstrated to induce ARL2 expression in MG-63 cells. We showed that miR-646 was downregulated in osteosarcoma specimens compared to that of non-tumor specimens and that the level of circ_0000527 was negatively correlated with miR-646 expression in osteosarcoma specimens. The elevated expression of circ_0000527 was shown to promote cell growth and cell cycle progression by modulating miR-646 expression. The ectopic expression of circ_0000527 was shown to promote cell growth, cell cycle progression and the secretion of inflammatory mediators by modulating ARL2. The present study suggested that the circ_0000527/miR-646/ARL2 axis may be a potential treatment target for osteosarcoma.