Long non-coding RNAs (lncRNAs) regulates the initiation and progression of osteosarcoma (OS), specifically lncRNA RP11-361F15.2 has been shown to play prominent roles in tumorigenesis. Previously, M2-Like polarization of tumor-associated macrophages (TAMs) has been identified to play a key role in cancer migration/invasion. Hence, it is essential to understand the role of RP11-361F15.2 in tumorigenesis and its association with M2-Like polarization of TAMs. The results indicate that RP11-361F15.2 is significantly increased in OS tissues, and its expression is positively correlated with cytoplasmic polyadenylation element binding protein 4 (CPEB4) expression and negatively associated with miR-30c-5p expression. Further, overexpression of RP11-361F15.2 increased OS cell migration/invasion and M2-Like polarization of TAMs in vitro, as well as promoted xenograft tumor growth in vivo. Mechanistically, luciferase reporter assays indicated that RP11-361F15.2 upregulated CPEB4 expression by competitively binding to miR-30c-5p. Further, we have identified that RP11-361F15.2 promotes CPEB4-mediated tumorigenesis and M2-Like polarization of TAMs through miR-30c-5p in OS. We also identified that RP11-361F15.2 acts as competitive endogenous RNA (ceRNA) against miR-30c-5p thereby binding and activating CPEB4. This RP11-361F15.2/miR-30c-5p/CPEB4 loop could be used as a potential therapeutic strategy for the treatment of OS.

中文翻译：

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LncRNA RP11-361F15.2通过抑制肿瘤相关的CPEB4巨噬细胞的M2极化来促进骨肉瘤的发生。

长的非编码RNA（lncRNA）调节骨肉瘤（OS）的起始和进展，特别是lncRNA RP11-361F15.2已显示在肿瘤发生中起重要作用。以前，已确定与肿瘤相关的巨噬细胞（TAM）的M2极化在癌症迁移/侵袭中起关键作用。因此，必须了解RP11-361F15.2在肿瘤发生中的作用及其与TAM的M2极化有关。结果表明，RP11-361F15.2在OS组织中显着增加，其表达与细胞质聚腺苷酸化元素结合蛋白4（CPEB4）表达正相关，而与miR-30c-5p表达负相关。此外，RP11-361F15.2的过度表达增加了TAM在体外的OS细胞迁移/侵袭和M2极化，并促进体内异种移植肿瘤的生长。从机理上讲，荧光素酶报告基因测定表明，RP11-361F15.2通过竞争性结合miR-30c-5p上调了CPEB4的表达。此外，我们已经确定，RP11-361F15.2通过OS中的miR-30c-5p促进CPEB4介导的TAM的肿瘤发生和M2极化。我们还确定RP11-361F15.2充当针对miR-30c-5p的竞争性内源RNA（ceRNA），从而结合并激活CPEB4。RP11-361F15.2 / miR-30c-5p / CPEB4环可用作OS的潜在治疗策略。2通过OS中的miR-30c-5p促进CPEB4介导的TAM的肿瘤发生和M2极化。我们还确定，RP11-361F15.2充当针对miR-30c-5p的竞争性内源RNA（ceRNA），从而结合并激活CPEB4。RP11-361F15.2 / miR-30c-5p / CPEB4环可用作OS的潜在治疗策略。2通过OS中的miR-30c-5p促进CPEB4介导的TAM的肿瘤发生和M2极化。我们还确定RP11-361F15.2充当针对miR-30c-5p的竞争性内源RNA（ceRNA），从而结合并激活CPEB4。RP11-361F15.2 / miR-30c-5p / CPEB4环可用作OS的潜在治疗策略。