Osteosarcoma (OS) is the most common primary malignant bone tumour with a peak in incidence during adolescence. Delayed patient presentation and diagnosis is common with approximately 15% of OS patients presenting with metastatic disease at initial diagnosis. With the introduction of neoadjuvant chemotherapy in the 1970s, disease prognosis improved from 17% to 60%‐70% 5‐year survival, but outcomes have not significantly improved since then. Novel and innovative therapeutic strategies are urgently needed as an adjunct to conventional treatment modalities to improve outcomes for OS patients. Angiogenesis is crucial for tumour growth, metastasis and invasion, and its prevention will ultimately inhibit tumour growth and metastasis. Dysregulation of angiogenesis in bone microenvironment involving osteoblasts and osteoclasts might contribute to OS development. This review summarizes existing knowledge regarding pre‐clinical and developmental research of targeted anti‐angiogenic therapy for OS with the aim of highlighting the limitations associated with this application. Targeted anti‐angiogenic therapies include monoclonal antibody to VEGF (bevacizumab), tyrosine kinase inhibitors (Sorafenib, Apatinib, Pazopanib and Regorafenib) and human recombinant endostatin (Endostar). However, considering the safety and efficacy of these targeted anti‐angiogenesis therapies in clinical trials cannot be guaranteed at this point, further research is needed to completely understand and characterize targeted anti‐angiogenesis therapy in OS.

The bystin-like (BYSL) gene is expressed in a wide range of eukaryotes and is closely associated with tumor progression. However, its function and mechanism in osteosarcoma remain unclear. Herein, the protein expression and clinical role of BYSL in human osteosarcoma tissues were assessed. High expression of BYSL was positively related to the metastasis status and poor patient prognosis. Mechanistically, upregulation of BYSL enhanced Nrf2 expression under hypoxia in osteosarcoma cells. MicroRNAs are important epigenetic regulators of osteosarcoma development. Noteworthy, bioinformatics analysis, dual-luciferase reporter and rescue assays showed that miR-378a-3p inhibited BYSL expression by binding to its 3′-untranslated region. Analysis of miR-378a-3p function under hypoxia and normoxia showed that its upregulation suppressed osteosarcoma cells invasion and inhibited epithelial-to-mesenchymal transition by suppressing BYSL. Collectively, the results show that the miR-378a-3p/BYSL may associate with metastasis risk in osteosarcoma.

Osteosarcoma (OS) is a primary bone tumor with high malignancy and the mechanism of hematogenous metastasis in OS is still not clear. The plasma exosomes derived from osteosarcoma play a key role in the process of tumor metastasis. Here, we established RNA-seq dataset for lncRNAs, circRNAs and mRNAs in plasma exosomes from 10 OS patients and 5 healthy donors. A total of 329.52 Gb of clean data was obtained. Besides, 1754 lincRNAs, 7096 known and 1935 new circRNA was identified. Finally, gene expression profiles and differentially expressed genes (DEGs) were analyzed among these 15 samples. There were 331 DEGs of mRNA, 132 of lincRNA and 489 of circRNA was obtained, respectively. This data set provides a significant resource for relevant researchers to excavate potential dysregulated lncRNAs, circRNAs and mRNAs of plasma exosomes in OS versus normal conditions.