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Spinal osteosarcoma (OS) is a rare and aggressive malignancy. Long noncoding RNA (lncRNA) BSN-AS2 has been shown to be an oncogenic gene in several cancers. However, the role and function of BSN-AS2 in spinal OS were unfamiliar. Our study identified that BSN-AS2 expression was boosted in spinal OS tissues and cell lines. Transcription factor E2F1 induced the upregulation of BSN-AS2 expression in spinal OS cells. Afterwards, loss-of-function assays indicated that BSN-AS2 depletion reduced cell proliferation, migration and invasion as well as promoted cell apoptosis in spinal OS. Thereafter, RIP, RNA pull down and luciferase reporter assays manifested BSN-AS2 could sponge miR-654-3p in spinal OS. After that, the binding effect of between miR-654-3p and SYTL2 was proved. Finally, rescue experiments illustrated that miR-654-3p inhibition or SYTL2 overexpression could counteract the inhibitory effect caused by BSN-AS2 deficiency on spinal OS progression. In conclusion, the availability of miR-654-3p was antagonized by E2F1-induced BSN-AS2 for SYTL2-meidated spinal OS progression.

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Chondrocyte apoptosis is an important factor in the development and progression of osteoarthritis (OA). Cryptotanshinone (CTS) can inhibit chondrocyte apoptosis, but the specific mechanism remains unknown. The aim of the present study was to explore how CTS may affect chondrocyte apoptosis. Reverse transcription-quantitative PCR and western blotting were used to validate microRNA (miR)-574-5p, YY1-associated factor 2 (YAF2), Bcl-2 and Bax expression levels. H&E, Safranin O and TUNEL staining assays were used to evaluate the apoptosis of arthritic chondrocytes in vivo . A Cell Counting Kit-8 assay and flow cytometry were performed to detect cell proliferation and apoptosis of chondrocytes in vitro . The methylation level of the miR-574-5p promoter was measured via methylation specific PCR. The degree of chondrocyte apoptosis and the expression levels of YAF2 and Bcl-2 were decreased in the mice with OA, and were increased in the OA + CTS mice, while the expression levels of miR-574-5p and Bax showed opposite changes. Furthermore, the degree of chondrocyte apoptosis and the expression levels of the aforementioned key factors in chondrocytes were consistent with those observed in vivo . The methylation degree of the miR-574-5p promoter was increased by the addition of CTS, and was reduced after the addition of a methylation inhibitor, 5-aza-CdR, indicating that CTS could regulate the methylation of miR-574-5p promoter. The present study suggested that CTS could downregulate the expression of miR-574-5p by regulating its methylation, and thus, could improve YAF2 expression and affect chondrocyte apoptosis.