MicroRNA-206 upregulation relieves circTCF25-induced osteosarcoma cell proliferation and migration.

Circular RNA TCF25 (circTCF25) has been proven to be upregulated in human malignancy and correlated with tumor process. Our study aimed to unravel whether circTCF25 dictates cellular activities of osteosarcoma cells and address the possible mechanisms associated with microRNA (miR). circTCF25 and miR-206 in clinical specimens from 25 patients suffering from osteosarcoma were quantified by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). circTCF25- or miR-206-overexpressed cells (MG-63 and Saos-2) were constructed by transfection and confirmed by qRT-PCR, and continually subjected to cascades of assays for viability by Cell Counting Kit-8, proliferation by BrdU+ , migration, and invasion by Transwell chamber and proteins involved in proliferation (cyclin D1 and CDK6), migration and invasion (MMPs, TIMP-1, and vimentin) and signaling transduction (mitogen-activated protein kinase [MEK], extracellular signal-regulated kinase [ERK], protein kinase B [AKT], mammalian target of rapamycin [mTOR]) by western blot. Targeting the relationship between miR-206 and circTCF25 was validated by the Dual-Luciferase Reporter System. circTCF25 was apparently enriched while miR-206 was deficient in osteosarcoma specimens. circTCF25 elevated viability, facilitated proliferation, and fortified migration and invasion capacities of MG-63 and Saos-2 cells. Besides, miR-206 was downregulated in circTCF25-replenished cells. However, miR-206 upregulation offset the carcinogenesis of circTCF25. miR-206 had the ability to downregulate circTCF25 by targeting it. Of note, circTCF25 drove the phosphorylation of signaling transducers while miR-206 upregulation relived the effect of circTCF25 on the phosphorylation. circTCF25 conferred carcinogenesis in osteosarcoma cells through and suppressing miR-206 expression. However, miR-206 overexpression buffered the carcinogenesis of circTCF25.