During the last decade, osteoarthritis (OA) has become one of the most prevalent musculoskeletal diseases worldwide. OA is characterized by progressive loss of articular cartilage, abnormal remodeling of subchondral bone, hyperplasia of synovial cells, and growth of osteophytes, which lead to chronic pain and disability. The pathological mechanisms underlying OA initiation and progression are still poorly understood. Non-coding RNAs (ncRNAs) constitute a large portion of the transcriptome that do not encode proteins but function in numerous biological processes. Cumulating evidence has revealed a strong association between the changes in expression levels of ncRNA and the disease progression of OA. Moreover, loss- and gain-of-function studies utilizing transgenic animal models have demonstrated that ncRNAs exert vital functions in regulating cartilage homeostasis, degeneration, and regeneration, and changes in ncRNA expression can promote or decelerate the progression of OA through distinct molecular mechanisms. Recent studies highlighted the potential of ncRNAs to serve as diagnostic biomarkers, prognostic indicators, and therapeutic targets for OA. MiRNAs and lncRNAs are two major classes of ncRNAs that have been the most widely studied in cartilage tissues. In this review, we focused on miRNAs and lncRNAs and provided a comprehensive understanding of their functional roles as well as molecular mechanisms in cartilage homeostasis and OA pathogenesis.

Background: β-catenin plays a crucial role in the progression of osteosarcoma. However, the clinical significance of β-catenin over-expression in osteosarcoma still remains unclear. Thus, we performed a meta-analysis of studies that evaluated the impact of β-catenin on metastasis and overall survival (OS) in osteosarcoma.Methods: We searched PubMed, The Cochrane Library, Embase, Springer, Science Direct, OVID, Weipu, Wanfang and China National Knowledge Internet (CNKI) databases from their start year up to Aug.2019. Individual hazard ratios (HRs) and 95% confidence intervals (CIs) were extracted and pooled HRs with 95% CIs or odd ratio (OR) were used to evaluate the relationships between β-catenin over-expression and metastasis and overall survival in osteosarcoma.Results: Eight related studies involving 521 patients were qualified for this meta-analysis. Results showed that over-expression of β-catenin was significantly correlated with metastasis (OR = 3.31, 95% CI = 2.08-5.24, P < 0.001) and overall survival (HR = 2.32, 95% CI = 1.48-363, P = 0.02). Conclusion:The meta-analysis revealed that over-expression of β-catenin might be associated with distant metastasis and overall survival in osteosarcoma, which reminds that β-catenin acts as a prognostic biomarker and it can guide the clinical therapy in osteosarcoma patients.

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Background and purpose: Osteosarcoma is the commonly seen type of primary malignant bone tumors in children and adolescents. Partial patients with osteosarcoma cannot tolerate the side effects of chemotherapy drugs. Hence, it is urgent to find anti-osteosarcoma drugs with low side effects. Melittin is an anti-tumor Traditional Chinese Medicine with low side effects. The purpose of this study was to explore the anti-osteosarcoma effect of melittin and its possible molecular mechanisms. Methods: The effects of melittin on cell growth were detected by CCK-8, clonal formation and flow cytometry. As well as the related molecules were investigated by Real-time PCR and Western blot. Xenograft model in nude mice was established to observe the effects of melittin on tumor growth and the related molecular expression were detected by immunohistochemistry. Results: Melittin can inhibit the proliferation of osteosarcoma 143B cells, reduce colony formation and induce apoptosis, while significantly up-regulate the expression of Bax and Caspase-3, and down-regulate the expression of Bcl-2 proteins. Moreover, treatment with melittin significantly reduced the mRNA and protein levels of β-catenin and Wnt/β-catenin related genes (LRP5, c-Myc, and Survivin) in osteosarcoma 143B cells in vitro. The xenograft model found that melittin significantly inhibited tumor growth and decreased the protein expression levels of β-catenin and Wnt/β-catenin related genes in vivo. Conclusion: These findings show that melittin could inhibit the growth of osteosarcoma 143B cells, which may be related to the inhibition of Wnt/β-catenin signaling pathway activity, and induce apoptosis by up-regulating the ratio of Bax/Bcl-2 in osteosarcoma 143B cells. Therefore, melittin is a promising anti-tumor drug for treatment of osteosarcoma.

This study aimed to identify co-expressed differentially expressed genes (DEGs) in quiescence and senescence of osteosarcoma (OS) U2OS cells and investigate their biological functions. GSE94805 from Gene Expression Omnibus database was extracted, involving 12 samples of OS U2OS cells (4 quiescence, 4 senescence, and 4 control samples). After analysis of DEGs by limma package, VENN analysis was performed to identify co-expressed DEGs in quiescence and senescent. The Cytoscape software was used to construct an interactive network of co-expressed DEGs. Finally, box-plot was drawn for the co-expressed DEGs in sub-network. Besides, the relation literatures were selected in GenCLiP database for the co-expressed DEGs. Seven hundred and forty-three DEGs (255 up-regulated genes, 488 down-regulated genes) were obtained in quiescence and 2135 DEGs (1189 up-regulated genes, 946 down-regulated genes) in senescence. Through VENN analysis, 448 DEGs (131 up-regulated genes, 317 down-regulated genes) were co-expressed in quiescent and senescence. In the co-expressed DEGs network, 896 nodes (448 nodes in quiescent, 448 nodes in senescent) were obtained. Finally, 16 co-expressed DEGs were obtained in the subnetwork analysis, in which Aurora kinase A (AURKA) and polo-like kinase (PLK4) had been reported in OS. AURKA and PLK4 might be the key genes in quiescence and senescence of OS U2OS cells.