Abstract Osteosarcoma (OS) is a common primary malignant bone tumor around the world. It has been reported that long noncoding RNAs (lncRNAs) take part in diverse pathological processes of OS; however, the mechanism remains unknown. This study aimed to uncover the profile of lncRNA small nucleolar RNA host gene 15 (SNHG15), its biological function, and its potential involvement in the mechanism of OS progression in vitro and in vivo. The expression of SNHG15 and TRAF4 was promoted in OS tissues opposite for that of miR-346. The silencing of SNHG15 limited the proliferation, invasion, and enhanced apoptosis of SaoS2 and HOS cells. Moreover, the putative binding sites between miR-346 and SNHG15 or TRAF4 were predicted by starBase and Targetscan software online, individually. Also, miR-346 deletion reversed the positive effects of SNHG15 elimination on proliferation, apoptosis, and invasion in cells. In addition, the upregulation of TRAF4 disrupted the biofunctional results from miR-346 promotion subsequently. Finally, SNHG15 knockdown repressed OS tumor growth in a xenograft tumor model. SNHG15 enhanced the progression of OS by regulating the miR-346/TRAF4 axis in vitro and in vivo.

中文翻译：

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LncRNA SNHG15通过海绵miR-346和调节TRAF4表达在体外和体内调节骨肉瘤进展

摘要 骨肉瘤（OS）是世界范围内常见的原发性恶性骨肿瘤。据报道，长链非编码 RNA (lncRNAs) 参与了 OS 的多种病理过程。然而，机制仍然未知。本研究旨在揭示 lncRNA 小核仁 RNA 宿主基因 15 (SNHG15) 的概况、其生物学功能及其在体外和体内 OS 进展机制中的潜在参与。SNHG15 和 TRAF4 在 OS 组织中的表达与 miR-346 的表达相反。SNHG15 的沉默限制了 SaoS2 和 HOS 细胞的增殖、侵袭和增强的凋亡。此外，通过starBase 和Targetscan 软件在线分别预测miR-346 和SNHG15 或TRAF4 之间的假定结合位点。还，miR-346 缺失逆转了 SNHG15 消除对细胞增殖、凋亡和侵袭的积极影响。此外，TRAF4 的上调随后破坏了 miR-346 促进的生物功能结果。最后，SNHG15 敲低抑制了异种移植肿瘤模型中的 OS 肿瘤生长。SNHG15 通过在体外和体内调节 miR-346/TRAF4 轴来增强 OS 的进展。