BackgroundMicroRNA-138 (miR-138) has been proven to be a tumor suppressor gene in various types of tumors. However, the expression and the role of miR-138 in human osteosarcoma are still poorly understood. We investigated the function and the underlying mechanism of miR-138 in osteosarcoma.MethodsThe expression of miR-138 in human osteosarcoma tissues and cell lines was detected by real-time PCR analysis. The gain-of-function and loss-of-function experiments were performed on osteosarcoma cell lines to investigate the effects of miR-138 on osteosarcoma progression, and to determine whether differentiated embryonic chondrocyte gene 2 (DEC2) mediates these effects. Cell proliferation, apoptosis and invasion were assessed by MTT, flow cytometry and transwell-matrigel assays. Dual-luciferase reporter assay was used to identify whether DEC2 is a direct target of miR-138.ResultsMiR-138 was significantly downregulated in human osteosarcoma tissues and cell lines. Moreover, miR-138 expression was significantly lower in metastatic osteosarcoma tissues than that in non-metastatic tissues. The in vitro gain-of-function and loss-of-function experiments demonstrated that miR-138 inhibited cell proliferation and invasion, and promoted cell apoptosis of human osteosarcoma cells. DEC2 was verified as a direct target of miR-138, and DEC2 could reverse the inhibitory effect of miR-138 on osteosarcoma progression.ConclusionsThese findings suggested that miR-138 acts as a tumor suppressor in osteosarcoma.miR-138 inhibited cell proliferation and invasion, as well as promoted cell apoptosis of human osteosarcoma cells, at least partially, by inhibiting the expression of DEC2. MiR-138/DEC2 may be a novel therapeutic target in osteosarcoma.
Chronic osteomyelitis is a bone infection that results in hypertrophic scarring of the soft tissue surrounding the infected bone. This scarring can create functional problems and its treatment is challenging. The aim of the present study was to evaluate the efficacy of decorin in treating scar formation in osteomyelitis and the underlying mechanism of its action. A rat osteomyelitis model was used, and animals were divided into three groups, as follows: Group A (control), group B (osteomyelitis model) and group C (decorin-treated). X-ray scans, hematoxylin and eosin (H&E) staining and Masson's trichrome staining were performed to observe changes in femur and muscle tissue. In order to assess the role of the transforming growth factor β1 (TGF-β1)/Smad signaling pathway in scar formation in osteomyelitis, alterations in muscle tissue morphology and in the activation of key members of the TGF-β1/Smad signaling pathway were investigated in groups A and B. According to the results of H&E staining, evident fibrosis in muscle tissue were observed at days 14 and 28 in group B. Simultaneously, the expression levels of key members of the TGF-β1/Smad signaling pathway were increased. Subsequent to treatment with decorin in group C, scarring was reduced, and significant downregulation of collagen I, TGF-β1, phosphorylated (p)Smad2 and pSmad3 protein expression levels was observed at days 14 and 28 compared with the osteomyelitis group. In conclusion, these results suggest that activation of TGF-β1 may serve an important role in the formation of scars in osteomyelitis and that decorin can reduce scar formation in an osteomyelitis rat model through inhibition of the TGF-β1/Smad signaling pathway.
The present study describes a safe anchor path of antegrade lag screw fixation in the posterior column. Insertion of the lag screws of adequate length is possible in the posterior column along its functional axis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.