Osteosarcoma (OS) is one of the most common types of primary bone tumors which poses negative effects on the bones of both young children and adolescents. LncRNA LINC00472 has been reported to be involved with poor prognostics in breast cancer and ovarian cancer. As a new lncRNA, its role in OS remains to be elusive. Herein, we are focused to explore its regulatory mechanism in the development of OS. qRT-PCR was utilized to examine the expressions of LINC00472 and miR-300 in OS tissues and cell lines. OS cell lines of U2OS and MG63 were used to investigate the biological function of LINC00472. Xenograft tumor model was built in nude mice with MG63 cells. The expressions of LINC00472 were inhibited in OS tissues and cells, and were negatively related to the expressions of miR-300. LINC00472 directly targeted miR-300. FOXO1 was inhibited in OS tissues and its expressions were negatively related to the expressions of miR-300. LINC00472 over-expressions decreased cell proliferation abilities and colony formation abilities. These effects were mediated by miR-300. The silence of LINC00472 and over-expressions of miR-300 suppressed FOXO1 expressions. LINC00472 greatly reduced tumor growth in vivo and this effect was attenuated by miR-300 mimic. From all the experiments and observations, we demonstrated that LINC00472 could be a potential tumor suppressor in OS through interacting with miR-300 and FOXO1.

中文翻译：

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LINC00472 的下调通过 miR-300 减少 FOXO1 表达促进骨肉瘤肿瘤发生


骨肉瘤（OS）是最常见的原发性骨肿瘤类型之一，对幼儿和青少年的骨骼造成负面影响。据报道，LncRNA LINC00472 与乳腺癌和卵巢癌的不良预后有关。作为一种新的lncRNA，它在OS中的作用仍然难以捉摸。在此，我们重点探讨其在操作系统发展中的调控机制。利用 qRT-PCR 检测 OS 组织和细胞系中 LINC00472 和 miR-300 的表达。 U2OS和MG63 OS细胞系用于研究LINC00472的生物学功能。 MG63细胞裸鼠建立异种移植瘤模型。 LINC00472在OS组织和细胞中的表达受到抑制，并且与miR-300的表达呈负相关。 LINC00472 直接靶向 miR-300。 FOXO1在OS组织中受到抑制，其表达与miR-300的表达呈负相关。 LINC00472 过度表达会降低细胞增殖能力和集落形成能力。这些作用是由 miR-300 介导的。 LINC00472 的沉默和 miR-300 的过度表达抑制了 FOXO1 的表达。 LINC00472 极大地减少了体内肿瘤的生长，并且这种效应被 miR-300 模拟物减弱。从所有的实验和观察中，我们证明 LINC00472 通过与 miR-300 和 FOXO1 相互作用可以成为 OS 中潜在的肿瘤抑制因子。