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Abstract：
The potential function and mechanism of circRNAs in regulating malignant performances of Osteosarcoma (OS) cells have not been well investigated. The expression level of CircLMO7, miR-21-5p and ARHGAP24 were detected by RT-qPCR. The relationship between miR-21-5p and circ-LMO7, as well as between miR-21-5p and ARHGAP24, was predicted and examined through bioinformatics analysis and luciferase reporter gene experiments. Moreover, OS cell growth, invasion, migration, and apoptosis were detected using the cell counting kit-8 (CCK-8), transwell and flow cytometry assays, respectively. ARHGAP24 protein level was measured using western blotting. In present study, we choose to investigate the role and mechanism of circ-LOM7 on OS cell proliferation, migration and invasion. circ-LOM7 was found to be down-regulated in OS tissues and cell lines. Enforced expression of circ-LOM7 suppressed the growth, invasion, and migration of OS cells. In contrast, decreasing circ-LMO7 expression had opposite effects. Furthermore, miR-21-5p was predicted to be sponged by circ-LMO7, and had an opposite role of circ-LMO7 in OS. Moreover, ARHGAP24 served as miR-21-5p\'s downstream target. Mechanistically, circ-LMO7 was packed in exosomes and acted as a cancer-suppresser on OS by sponging miR-21-5p and upregulating the expression of ARHGAP24. The exosomal circ-LMO7 expression was significantly decreased in OS cell exosomes, and co-culture experiments showed that exosomal circ-LMO7 suppressed the proliferation ability of OS cells. Circ-LMO7 exerts as a tumor suppressor in OS, and the circ-LMO7/miR-21-5P/ARHGAP24 axis is involved in OS progression.
摘要：
circRNAs在调节骨肉瘤（OS）细胞恶性表现中的潜在功能和机制尚未得到很好的研究。RT-qPCR检测CircLMO7、miR-21-5p和ARHGAP24的表达水平。通过生物信息学分析和荧光素酶报告基因实验对miR-21-5p与circ-LMO7之间以及miR-21-5p与ARHGAP24之间的关系进行了预测和检查。此外，OS细胞生长，入侵,迁移,细胞计数试剂盒-8（CCK-8）检测细胞凋亡，transwell和流式细胞术分析，分别。使用蛋白质印迹法测量ARHGAP24蛋白水平。在目前的研究中,我们选择研究circ-LOM7对OS细胞增殖的作用和机制，移民和入侵。发现circ-LOM7在OS组织和细胞系中下调。circ-LOM7的强制表达抑制了生长，入侵,和OS细胞的迁移。相比之下,降低circ-LMO7表达具有相反的作用。此外，预测miR-21-5p被circ-LMO7海绵化,并且在OS中具有与circ-LMO7相反的作用。此外，ARHGAP24作为miR-21-5p的下游靶标。机械上,circ-LMO7被包装在外泌体中，并通过膨胀miR-21-5p和上调ARHGAP24的表达而充当OS的癌症抑制剂。OS细胞外泌体circ-LMO7表达显著降低,共培养实验表明，外泌体circ-LMO7抑制OS细胞的增殖能力。Circ-LMO7在OS中作为肿瘤抑制因子发挥作用，circ-LMO7/miR-21-5P/ARHGAP24轴参与OS进展。
