Despite great advances have been made in the understanding of biology of osteosarcoma, the molecular mechanisms involved in osteosarcoma tumorigenesis and progression are still largely unknown. Long noncoding RNA (lncRNA) is a new type of RNA molecule, which plays pivotal roles in many tumors. lncRNA BCAR4 has been identified as an oncogenetic lncRNA involved in the progression of breast cancer. However, the functions and clinical significances of BCAR4 in osteosarcoma are unknown now. In this study, we found that BCAR4 was significantly upregulated in osteosarcoma tissues. Increased expression of BCAR4 was significantly correlated with large tumor size, advanced Enneking stage, lung metastasis, and poor prognosis. Functional experiments demonstrated that knockdown of BCAR4 inhibits the proliferation and migration of osteosarcoma cell in vitro. Consistently, knockdown of BCAR4 inhibits osteosarcoma tumorigenesis and lung metastasis in vivo. Chromatin isolation by RNA purification assay showed that BCAR4 physically associates with the promoters of GLI2 target genes. The depletion of BCAR4 inhibits the expression of GLI2 target genes and GLI2 reporter luciferase activity in a dose-dependent manner. The expression of BCAR4 and GLI2 target genes is significantly correlated in osteosarcoma tissues. Depletion of DLI2 abolished the effects of BCAR4 on osteosarcoma. Taken together, these findings demonstrated that BCAR4 promotes osteosarcoma progression via activating GLI2-dependent gene transcription and serves as a potential prognostic biomarker and a therapeutic target of osteosarcoma.

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Background This study investigates whether three-dimensional (3D) printing-assisted revision total hip/knee arthroplasty could improve its clinical and radiological outcomes and assess the depth and breadth of research conducted on 3D printing-assisted revision total hip and knee arthroplasty. Methods A literature search was carried out on PubMed, Web of Science, EMBASE, and the Cochrane Library. Only studies that investigated 3D printing-assisted revision total hip and knee arthroplasty were included. The author, publication year, study design, number of patients, patients’ age, the time of follow-up, surgery category, Coleman score, clinical outcomes measured, clinical outcomes conclusion, radiological outcomes measured, and radiological outcomes conclusion were extracted and analyzed. Results Ten articles were included in our review. Three articles investigated the outcome of revision total knee arthroplasty, and seven investigated the outcome of revision total hip arthroplasty. Two papers compared a 3D printing group with a control group, and the other eight reported 3D printing treatment outcomes alone. Nine articles investigated the clinical outcomes of total hip/knee arthroplasty, and eight studied the radiological outcomes of total hip/knee arthroplasty. Conclusion 3D printing is being introduced in revision total hip and knee arthroplasty. Current literature suggests satisfactory clinical and radiological outcomes could be obtained with the assistance of 3D printing. Further long-term follow-up studies are required, particularly focusing on cost-benefit analysis, resource availability, and, importantly, the durability and biomechanics of customized prostheses using 3D printing compared to traditional techniques.

Background: Accumulating evidence demonstrates that long non-coding RNAs (lncRNAs) are associated with the development of osteoporosis. The present study aimed to investigate the effect of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on osteogenic differentiation in osteoporosis.Methods: MALAT1 levels were detected by a real-time polymerase chain reaction (RT-qPCR). Moreover, the levels of osteogenic differentiation-related factors (Bmp4, Col1a1 and Spp1) were measured by a RT-qPCR and western blotting. Alkaline phosphatase (ALP) activity was detected using an ALP staining assay.Results: MALAT1 levels were downregulated in hindlimb unloading mice and simulated in microgravity (MG) treated MC3T3-E1 cells. Moreover, MG treatment induced the downregulation of the expression of ALP, BMP4, Col1a1 and Spp1, whereas overexpression of MALAT1 abolished the downregulation. MG also inhibited ALP activity, whereas MALAT1 reversed the effect. Furthermore, miR-217 was identified as a target of MALAT1, and AKT3 was verified as a target of miR-217.Overexpression of miR-217 rescued the promotion of osteogenic differentiation induced by MALAT1 in MG treated cells. Knockdown of AKT3 abolished the facilitation of osteogenic differentiation induced by downregulation of miR-217.Conclusions: MALAT1 promotes osteogenic differentiation through regulating miR-217/AKT3 axis, suggesting that MALAT1 is a potential target with respect to alleviating osteoporosis.