Long non-coding RNAs (lncRNAs) have been characterized by playing a crucial role in tumorigenesis. However, the detail biological function and clinical importance of lncRNAs in colorectal cancer (CRC) are unclear and have attracted different levels of in-depth research. In this context, we explored the differentially expressed profiles of lncRNAs in six CRC tissues and three adjacent non-tumor tissues from RNA-sequencing (RNA-seq) study and noted a lncRNA, RP11-51O6.1, which is markedly overexpressed in CRC tissues, particularly in aggressive cases. Impressively, an elevated RP11-51O6.1 level was highly correlated with poor prognosis in clinical patients. Functional analyses revealed that RP11-51O6.1 could promote cell proliferation in vitro and in vivo. Furthermore, we reported that RP11-51O6.1 enhances cell migration and invasion in vitro. Mechanistic studies (Bioinformatics binding site analyses, the Luciferase reporter, Ago2 immunoprecipitation, the RNA pull-down, immunofluorescence colocalization, rescued assays and western blotting) implicated that RP11-51O6.1 could regulate YAP1 expression by competitively sponging miR-206 and blocking its activity in promoting CRC progression. Conclusively, our findings identify a novel RP11-51O6.1/miR-206/YAP1 regulatory axis that participates in CRC progression and development, suggesting RP11-51O6.1 is an exploitable biomarker and appealing therapeutic target in treating CRC.

中文翻译：

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RP11-51O6.1 海绵 miR-206 通过上调 YAP1 加速结直肠癌的癌变和转移。

长链非编码 RNA (lncRNA) 的特点是在肿瘤发生中起着至关重要的作用。然而，lncRNAs在结直肠癌（CRC）中的详细生物学功能和临床重要性尚不清楚，并引起了不同程度的深入研究。在此背景下，我们从 RNA 测序 (RNA-seq) 研究中探索了 6 个 CRC 组织和 3 个相邻非肿瘤组织中 lncRNA 的差异表达谱，并注意到 lncRNA RP11-51O6.1 在 CRC 中显着过表达组织，特别是在侵袭性病例中。令人印象深刻的是，升高的 RP11-51O6.1 水平与临床患者的不良预后高度相关。功能分析表明，RP11-51O6.1 可以促进体外和体内细胞增殖。此外，我们报道了 RP11-51O6.1 增强了体外细胞迁移和侵袭。机制研究（生物信息学结合位点分析、荧光素酶报告基因、Ago2 免疫沉淀、RNA 下拉、免疫荧光共定位、拯救分析和蛋白质印迹）表明 RP11-51O6.1 可以通过竞争性海绵 miR-206 并阻断其来调节 YAP1 表达促进 CRC 进展的活性。总之，我们的研究结果确定了一个新的 RP11-51O6.1/miR-206/YAP1 调节轴，它参与了 CRC 的进展和发展，表明 RP11-51O6.1 是一种可利用的生物标志物和有吸引力的治疗 CRC 的治疗靶点。1 可以通过竞争性海绵 miR-206 并阻断其促进 CRC 进展的活性来调节 YAP1 表达。总之，我们的研究结果确定了一个新的 RP11-51O6.1/miR-206/YAP1 调节轴，它参与了 CRC 的进展和发展，表明 RP11-51O6.1 是一种可利用的生物标志物和有吸引力的治疗 CRC 的治疗靶点。1 可以通过竞争性海绵 miR-206 并阻断其促进 CRC 进展的活性来调节 YAP1 表达。总之，我们的研究结果确定了一个新的 RP11-51O6.1/miR-206/YAP1 调节轴，它参与了 CRC 的进展和发展，表明 RP11-51O6.1 是一种可利用的生物标志物和有吸引力的治疗 CRC 的治疗靶点。