Abstract

Osteosarcoma (OS) is known as a tumor that derives from skeletal system with increasing incidence worldwide. This study aimed to explore the effect of a circular RNA (circRNA), circ_0102049, on OS and reveal its potential molecular mechanism. In this work, the expression of circ_0102049 was detected by quantitative real time polymerase chain reaction (qRT-RCR) in both OS specimens and cell lines. The relationship between circ_0102049 level and patients’ overall survival was evaluated by Kaplan-Meier curves and Cox regression analysis. Cell proliferation, apoptosis, migration and invasion of U2OS and MG63 cells were measured by cell counting kit-8 (CCK-8), flow cytometry, wound healing and transwell experiments, respectively. In addition, subcellular fractionation, bioinformatics analysis and dual-luciferase reporter assay were utilized to reveal the mechanism of circ_0102049 in OS. Circ_0102049 was overexpressed in both OS specimens and cells. Moreover, the level of circ_0102049 in OS patients was markedly correlated with larger tumor size, pulmonary metastasis and poor prognosis. Circ_0102049 remarkably accelerated cell proliferation, migration and invasion but attenuated cell apoptosis in OS cells analyzed by gain/loss of function experiments. What’s more, we identified that circ_0102049 functions as a competing endogenous RNA (ceRNA) to competitively sponge miR-1304-5p to upregulate MDM2 expression at posttranscriptional level, thus mediating the cellular behaviors of OS cells. Collectively, our study provides an innovatively regulatory mechanism of circ_0102049 in OS and points out a new way for OS treatment.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.