Studies have reported frequent downregulation of microRNA-125-5p (miR-125) in osteosarcoma tissues. However, the molecular role and mechanism of action of miR-125-5p in osteosarcoma via regulation of Kruppel-like factor 13 (KLF13) is yet to be explored. The results of the present study miR-125-5p are significantly (P < .05) downregulated in human osteosarcoma tissues and cell lines. Overexpression of miR-125-5p resulted in a significant (P < .5) decrease of the osteosarcoma cells via induction of autophagy. Additionally, overexpression of miR-125-5p also decreased the migration and invasive potential of the osteosarcoma cells. Bioinformatic analysis and dual-luciferase assays revealed that miR-125-5p targets KLF13. Post-transcriptional suppression of KLF13 by miR-125-5p results in the inhibition of osteosarcoma cells. Nonetheless, overexpression of KLF13 could abolish the tumor-suppressive effects of miR-125-5p. Taken together, these results suggest the tumor-suppressive role of miR-125-5p in and point toward its therapeutic potential in the treatment of osteosarcoma.

研究报道骨肉瘤组织中的microRNA-125-5p（miR-125）频繁下调。然而，miR-125-5p通过调节Kruppel样因子13（KLF13）在骨肉瘤中的分子作用和作用机理尚待探索。本研究的结果miR-125-5p 在人骨肉瘤组织和细胞系中显着下调（P <.05）。miR-125-5p的过度表达导致显着（P <.5）通过自噬诱导骨肉瘤细胞减少。另外，miR-125-5p的过表达也降低了骨肉瘤细胞的迁移和侵袭潜能。生物信息学分析和双荧光素酶测定法表明miR-125-5p靶向KLF13。miR-125-5p对KLF13的转录后抑制导致骨肉瘤细胞的抑制。但是，KLF13的过表达可以消除miR-125-5p的肿瘤抑制作用。综上所述，这些结果表明miR-125-5p在骨肉瘤的治疗中具有肿瘤抑制作用，并指出了其在骨肉瘤治疗中的治疗潜力。