Background Accumulating evidence has associated aberrant long non-coding RNAs (lncRNAs) with various human cancers. This study aimed to explore the role of LINC00908 in prostate cancer (PCa) and its possible underlying mechanisms. Methods Microarray data associated with PCa were obtained from the Gene Expression Omnibus (GEO) to screen the differentially expressed genes or lncRNAs. Then, the expression of LINC00908 in PCa tissues and cell lines was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The localization of LINC00908 in PCa cells was examined by fluorescence in situ hybridization (FISH). The relationship among LINC00908, microRNA (miR)-483-5p, and TSPYL5 was detected by bioinformatics analysis, dual-luciferase reporter assay, RNA pull-down, RNA binding protein immunoprecipitation (RIP), and FISH assays. Cell biological behaviors were assessed after the expression of LINC00908, miR-483-5p, and TSPYL5 was altered in PCa cells. Lastly, tumor growth in nude mice was evaluated. Results Poorly expressed LINC00908 was witnessed in PCa tissues and cells. LINC00908 competitively bound to miR-483-5p to up-regulate the TSPYL5 expression. Overexpression of LINC00908 resulted in reduced PCa cell proliferation, migration and invasion, and promoted apoptosis. Additionally, the suppression on PCa cell proliferation, migration and invasion was induced by up-regulation of TSPYL5 or inhibition of miR-483-5p. In addition, in vivo experiments showed that overexpression of LINC00908 inhibited tumor growth of PCa. Conclusion Overall, LINC00908 could competitively bind to miR-483-5p to increase the expression of TSPYL5, thereby inhibiting the progression of PCa. Therefore, LINC00908 may serve as a novel target for the treatment of PCa.

中文翻译：

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LINC00908 负调节 microRNA-483-5p 以增加 TSPYL5 表达并抑制前列腺癌的发展。

背景 越来越多的证据表明异常长链非编码 RNA (lncRNA) 与各种人类癌症有关。本研究旨在探讨 LINC00908 在前列腺癌 (PCa) 中的作用及其可能的潜在机制。方法 从 Gene Expression Omnibus (GEO) 获得与 PCa 相关的微阵列数据，以筛选差异表达的基因或 lncRNA。然后，通过逆转录-定量聚合酶链反应 (RT-qPCR) 检测 LINC00908 在 PCa 组织和细胞系中的表达。通过荧光原位杂交 (FISH) 检查 LINC00908 在 PCa 细胞中的定位。通过生物信息学分析、双荧光素酶报告基因分析、RNA pull-down、RNA 结合蛋白免疫沉淀 (RIP) 和 FISH 分析检测 LINC00908、microRNA (miR)-483-5p 和 TSPYL5 之间的关系。在 PCa 细胞中改变 LINC00908、miR-483-5p 和 TSPYL5 的表达后评估细胞生物学行为。最后，评估了裸鼠中的肿瘤生长。结果 LINC00908在PCa组织和细胞中表达不佳。LINC00908 与 miR-483-5p 竞争性结合以上调 TSPYL5 表达。LINC00908 的过表达导致 PCa 细胞增殖、迁移和侵袭减少，并促进细胞凋亡。此外，上调 TSPYL5 或抑制 miR-483-5p 可诱导 PCa 细胞增殖、迁移和侵袭的抑制。此外，体内实验表明，LINC00908 的过表达抑制了 PCa 的肿瘤生长。结论 总体而言，LINC00908可与miR-483-5p竞争性结合，增加TSPYL5的表达，从而抑制PCa的进展。