BACKGROUND Accumulating evidence indicates that aberrant microRNA (miRNA) expression contributes to osteosarcoma progression. This study aimed to elucidate the association between miR-624-5p expression and osteosarcoma (OS) development and to investigate its underlying mechanism. METHODS We analyzed GSE65071 from the GEO database and found miR-624-5p was the most upregulated miRNA. The expression of miR-624-5p and its specific target gene were determined in human OS specimens and cell lines by RT-PCR and western blot. The effects of miR-624-5p depletion or ectopic expression on OS proliferation, migration and invasion were evaluated in vitro using CCK-8 proliferation assay, colony formation assay, transwell assay, would-healing assay and 3D spheroid BME cell invasion assay respectively. We investigated in vivo effects of miR-624-5p using a mouse tumorigenicity model. Besides, luciferase reporter assays were employed to identify interactions between miR-624-5p and its specific target gene. RESULTS miR-624-5p expression was upregulated in OS cells and tissues, and overexpressing miR-624-5p led to a higher malignant level of OS, including cell proliferation, migration and invasion in vitro and in vivo. Protein tyrosine phosphatase receptor type B (PTPRB) was negatively correlated with miR-624-5p expression in OS tissues. Using the luciferase reporter assay and Western blotting, PTPRB was confirmed as a downstream target of miR-624-5p. PTPRB restored the effects of miR-624-5p on OS migration and invasion. The Hippo signaling pathway was identified as being involved in the miR-624-5p/PTPRB axis. CONCLUSIONS In conclusion, our results suggest that miR-624-5p is a negative regulator of PTPRB and a risk factor for tumor metastasis in OS progression.

中文翻译：

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miR-624-5p通过靶向骨肉瘤细胞中的PTPRB抑制河马信号传导，从而促进肿瘤发生和转移。

背景技术越来越多的证据表明异常的microRNA（miRNA）表达有助于骨肉瘤的进展。这项研究旨在阐明miR-624-5p表达与骨肉瘤（OS）发育之间的关联并研究其潜在机制。方法我们从GEO数据库中分析了GSE65071，发现miR-624-5p是上调程度最高的miRNA。通过RT-PCR和western blot检测miR-624-5p及其特异性靶基因在人OS标本和细胞系中的表达。分别使用CCK-8增殖测定，集落形成测定，transwell测定，意愿修复测定和3D球形BME细胞侵入测定，在体外评估miR-624-5p耗竭或异位表达对OS增殖，迁移和侵袭的影响。我们使用小鼠致瘤性模型研究了miR-624-5p的体内作用。此外，萤光素酶报告基因测定被用于鉴定miR-624-5p与其特异性靶基因之间的相互作用。结果miR-624-5p在OS细胞和组织中的表达上调，并且过表达miR-624-5p导致OS的恶性程度更高，包括细胞增殖，在体内外的迁移和侵袭。B蛋白酪氨酸磷酸酶受体（PTPRB）与OS组织中miR-624-5p表达负相关。使用荧光素酶报告基因测定和蛋白质印迹，证实PTPRB是miR-624-5p的下游靶标。PTPRB恢复了miR-624-5p对OS迁移和入侵的影响。Hippo信号通路被确定与miR-624-5p / PTPRB轴有关。结论总而言之，