Vascular endothelial growth factor (VEGF) A and vascular endothelial growth factor receptor 1 (VEGFR1) signaling is crucial for angiogenesis and progression of osteosarcoma (OS). However, the regulation of the VEGF/VEGFR1 expression is still unclear in OS. Here, we show lower levels of miRNA-134 (miR-134) in OS tissues and cells. Induction of miR-134 overexpression significantly reduced the proliferation of Saos-2 cells and their secretion of pro-angiogenic factors, but increased the frequency of apoptotic Saos-2 cells. Treatment with conditioned medium from the cells transfected with miR-134 reduced the tube formation in human umbilical vein endothelial cells, which was abrogated by a combination of VEGF and conditioned medium. Furthermore, miR-134 significantly inhibited the growth of implanted OS tumors in vivo and attenuated the VEGFA and VEGFR1 expression and angiogenesis in the tumors. In addition, higher levels of VEGFA and VEGFR1 were detected and miR-134 inhibited the expression of VEGFA and VEGFR1 in Saos-2 cells and OS tumors. Bioinformatic analysis indicated that the 3'-UTR of VEGFA and VEGFR1 contained the motif for miR-134 binding. Co-transfection with the luciferase reporter containing the wild-type, but not the mutant, of the 3'-UTR of VEGFA or VEGFR1 together with miR-134 decreased the luciferase activity in Saos-2 cells. Finally, miR-134 dramatically inhibited AKT activation and proliferating cell nuclear antigen expression in Saos-2 cells. Collectively, these findings indicate that miR-134 is a potential tumor suppressor by targeting VEGFA/VEGFR1 signaling to attenuate the progression and angiogenesis in OS. Therefore, miR-134 may be a novel biomarker for the prognosis of OS and a target for the design of new therapies for OS.

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The relationship between pore architecture and structure performance needs to be explored, as well as confirm the optimized porous structure. Because of the linear correlation between constant C and pore architecture, triply periodic minimal surface (TPMS) based porous structures could be a controllable model for the investigation of the optimized porous structure. In the present work, three types of TPMS porous scaffolds (S, D and G) combined with four constants (0.0, 0.2, 0.4 and 0.6) were designed, and built successfully via the selective laser melting (SLM) technology. The designed feature and mechanical property of porous scaffolds were investigated through mathematical method and compression test. And the manufactured samples were co-cultured with rMSCs for the compatibility study. The results indicated that the whole manufacturing procedure was good in controllability, repeatability, and accuracy. The linear correlation between the porosity of TPMS porous scaffolds and the constant C in equations was established. The different TPMS porous scaffolds possess the disparate feature in structure, mechanical property and cell compatibility. Comprehensive consideration of the structure features, mechanical property and biology performance, different TPMS structures should be applied in appropriate field. The results could guide the feasibility of apply the different TPMS architectures into the different part of orthopedic implants.

Because of the modest response rate after surgery and chemotherapy, treatment of osteosarcoma (OS) remains challenging due to tumor recurrence and metastasis. miR-135a has been reported to act as an anticarcinogenic regulator of several cancers. However, its expression and function in osteosarcoma remain largely unknown. Here, we reported that abridged miR-135a expression in OS cells and tissues, and its expression is inversely correlated with the expression of BMI1 and KLF4, which are described as oncogenes in several cancers. Ectopic expression of miR-135a inhibited cell invasion and expression of BMI1 and KLF4 in OS cells. In vivo investigation confirmed that miR-135a acts as a tumor suppressor in OS to inhibit tumor growth and lung metastasis in xenograft nude mice. BMI1 and KLF4 were revealed to be direct targets of miR-135a, and miR-135a had a similar effect as the combination of si-BMI1 and si-KLF4 on inhibiting tumor progression and the expression of BMI1 and KLF4 in vivo. Altogether, our results demonstrate that the targeting of BMI1/KLF4 with miR-135a may provide an applicable strategy for exploring novel therapeutic approaches for OS.

Ollier disease, also known as multiple enchondromatosis, is a rare congenital disease of unknown etiology. The main manifestation of this disease is a non-ossifying chondrocyte mass or hamartomatous growth of a chondrocyte in the metaphysis. A few cases can develop into chondrosarcoma or osteosarcoma. The present study describes the case of a 37-year-old male patient with left hip pain and dyskinesia diagnosed with Ollier disease, according to clinical features and findings of imaging analysis. In general, the incidence of Ollier disease is low, and thus, it is not well-known among orthopedic surgeons. However, due to its malignant transformation rate, medical practitioners should encourage patients to undergo regular follow-up examinations. In an aim to provide some insight into this disease, the present study begins by describing the case of an affected patient case and subsequently presents a review of the relevant literature in order to guide the clinical diagnosis and treatment of the disease.