No abstract

Osteosarcoma (OS) is a common malignant bone tumor that is mainly found in the limbs, but can also appear in the axial skeleton. 1 OS occurs primarily in children and adolescents 15-25 years of age. 2 OS has high malignancy, and the main treatment is surgery combined with neoadjuvant radiotherapy and chemotherapy. 3 However, the 5 year survival rate has not substantially improved in the past few decades. Consequently, a greater understanding of the underlying molecular mechanism is needed to provide more effective clinical treatment methods.Long non-coding RNAs (lncRNAs) are transcripts greater than 200 bp in length with no protein-coding ability. LncRNAs influence the transcription and translation of some genes through

Background MiR-1297 is reported to function as a tumor suppressor of various cancers. However, the role of miR-1297 in the development of osteosarcoma (OS) has not been elaborated. The purpose of this study was to investigate the functional effects of miR-1297 on OS progression and the underlying mechanism. Methods The expression of protein and mRNA in OS cells was evaluated by Western blotting and quantitative real-time polymerase chain reaction. Cellular proliferation was investigated by cell counting kit-8, colony formation and apoptosis assays. Bioinformatics methods were used to predict target genes. The relationship between PFKFB2 and miR-1297 was demonstrated by dual-luciferase reporter assay. Metabolic changes in OS cells were monitored using an XF96 metabolic flux analyzer. Results We found that miR-1297 was downregulated in OS and that lower expression of miR-1297 promoted proliferation and contributed to the Warburg effect in OS cells. Furthermore, we showed that silencing PFKFB2 inhibited proliferation and reduced aerobic glycolysis while overexpression of PFKFB2 reduced the anti-tumor function of miR-1297 in OS cells. Mechanistically, miR-1297 acted as a tumor suppressor in OS and reduced the expression of PFKFB2 by directly targeting its 3ʹUTR. Conclusion The miR-1297 / PFKFB2 axis regulated OS proliferation by controlling the Warburg effect. Our results revealed a previously undiscovered function of miR-1297 in OS, which strongly linked metabolic alterations with cancer progression. Targeting miR-1297 may become a promising therapeutic approach for OS.