Long noncoding RNA (lncRNA) dysregulation is known to be taking part in majority of cancers, including osteosarcoma. In one of our previous studies, we showed that lncRNA MEG3 is being regulated by microRNA‐664a (miR‐664a) suppresses the migratory potential of osteosarcoma cells (U‐2OS). We now report a novel lncRNA, namely, ERICD, which is linked to the transcription factor AT‐rich interaction domain 3A (ARID3A) in U‐2OS cells. We show that ARID3A binds to ERICD and indirectly interacts with each other via the E2F transcription factor 1 (E2F1). Furthermore, small interfering RNA (siRNA)‐mediated knockdown of ERICD inhibited cell migration, formation of colonies, and proliferation in U‐2OS cells. Overexpression of ARID3A inhibited cell migration, colony formation, and proliferation, whereas siRNA‐mediated knockdown of ARID3A promoted cell migration, colony formation, and proliferation. Our findings indicate that ARID3A and lncRNA ERICD have plausible tumor suppressive and oncogenic functions, respectively, in osteosarcoma. Our data demonstrate the converse interaction between ARID3A and lncRNA ERICD that target DNA‐binding proteins and dysregulation of their expression through E2F1 augments osteosarcoma progression. The cell rescue experiment also indicated E2F1 to be involved in the regulation of ARID3A and ERICD.

中文翻译：

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长非编码RNA ERICD通过E2F1与ARID3A相互作用，并调节骨肉瘤细胞的迁移和增殖。

长期的非编码RNA（lncRNA）失调是包括骨肉瘤在内的大多数癌症的原因。在我们之前的一项研究中，我们表明lncRNA MEG3受microRNA-664a（miR-664a）的调节可抑制骨肉瘤细胞（U-2OS）的迁移潜能。现在我们报告一种新型的lncRNA，即ERICD，它与U-2OS细胞中的转录因子AT富集相互作用域3A（ARID3A）相链接。我们表明，ARID3A绑定到ERICD，并通过E2F转录因子1（E2F1）彼此间接相互作用。此外，小干扰RNA（siRNA）介导的ERICD的敲低抑制了U-2OS细胞中的细胞迁移，集落形成和增殖。ARID3A的过表达抑制细胞迁移，集落形成和增殖，siRNA介导的ARID3A敲低促进了细胞迁移，集落形成和增殖。我们的发现表明，ARID3A和lncRNA ERICD在骨肉瘤中分别具有合理的抑癌和致癌作用。我们的数据证明了靶向DNA结合蛋白的ARID3A和lncRNA ERICD之间的逆向相互作用以及通过E2F1对其表达的失调促进了骨肉瘤的进展。细胞抢救实验还表明E2F1参与了ARID3A和ERICD的调控。我们的数据证明了靶向DNA结合蛋白的ARID3A和lncRNA ERICD之间的逆向相互作用以及通过E2F1对其表达的失调促进了骨肉瘤的进展。细胞抢救实验还表明E2F1参与了ARID3A和ERICD的调控。我们的数据证明了靶向DNA结合蛋白的ARID3A和lncRNA ERICD之间的逆向相互作用以及通过E2F1对其表达的失调促进了骨肉瘤的进展。细胞抢救实验还表明E2F1参与了ARID3A和ERICD的调控。