Taken together, these findings will shed light on the role and mechanism of miR-133b in regulating osteosarcoma cell growth via the miR-133b/Sirt1 axis, and miR-133b may serve as a potential therapeutic target in osteosarcoma in the future.
The endogenous expression level of miR-133b is sufficient for inducing cisplatin resistance, which suggests that miR-133b may be a biomarker for cisplatin resistance in osteosarcoma.
miR-133b was significantly down-regulated while FGFR1 robustly up-regulated in OS tissues and OS cell lines, when compared to normal bone tissues and normal osteoblasts, respectively.
Our data assessed specific miRNA profiling deregulation in OS clinical samples and suggest that the expression of miR-1 and miR-133b may control cell proliferation and cell cycle through MET protein expression modulation.
Our results, although obtained in a small series of cases, confirming the high molecular homology with human OS suggesting a potential role of miR-1 and miR-133b as biomarkers for canine OS treatment.
This study provides a new insight into miRNAs dysregulation in osteosarcoma, and indicates that miR-133b may play as a tumor suppressor gene in osteosarcoma.