Long non-coding RNAs (lncRNAs) biological functions and molecular mechanisms associated with pancreatic cancer (PC) remain to be poorly elucidated. We aimed to clarify the role of lncRNA LINC00261 (LINC00261) in PC and confirm its regulatory mechanisms. Bioinformatics analysis, RNA pull-down and RIP assays were performed to investigate relationship between LINC00261 and forkhead box P3 (FOXP3). Further, dual-luciferase reporter gene and ChIP assays were employed to confirm the relationship among LINC00261, FOXP3 and sterol carrier protein-2 (SCP2). PC cells were introduced with a series of vectors to verify the effects of LINC00261 and SCP2 on the viability, cell cycle progression, migration and angiogenesis of PC cells. Nude mice with the xenograft tumour were used to evaluate the effects LINC00261 on the tumourigenicity. LINC00261 was lowly expressed in PC tissues and cells. SCP2 was inhibited by LINC00261 through FOXP3. Functionally, upregulated LINC00261 or downregulated SCP2 led to reduced cell viability, migration, angiogenesis and tumourigenicity potentials. This study demonstrated the inhibitory role of LINC00261 in the angiogenesis and cell cycle progression of PC cells. It acts through the negative regulation of SCP2 via targeting FOXP3. Findings in this study highlight a potentially biomarker for PC treatment.

中文翻译：

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LINC00261 升高通过靶向 FOXP3 上调 SCP2 来抑制胰腺癌细胞的血管生成和细胞周期进程

与胰腺癌 (PC) 相关的长链非编码 RNA (lncRNA) 生物学功能和分子机制仍不清楚。我们旨在阐明 lncRNA LINC00261 (LINC00261) 在 PC 中的作用并确认其调控机制。进行生物信息学分析、RNA 下拉和 RIP 分析以研究 LINC00261 和叉头盒 P3 (FOXP3) 之间的关系。此外，采用双荧光素酶报告基因和 ChIP 测定来确认 LINC00261、FOXP3 和甾醇载体蛋白-2 (SCP2) 之间的关系。向 PC 细胞引入一系列载体，以验证 LINC00261 和 SCP2 对 PC 细胞活力、细胞周期进程、迁移和血管生成的影响。具有异种移植肿瘤的裸鼠用于评估LINC00261对致瘤性的影响。LINC00261 在 PC 组织和细胞中低表达。SCP2 被 LINC00261 通过 FOXP3 抑制。在功能上，上调的 LINC00261 或下调的 SCP2 导致细胞活力、迁移、血管生成和致瘤潜能降低。本研究证明了 LINC00261 在 PC 细胞的血管生成和细胞周期进程中的抑制作用。它通过针对 FOXP3 对 SCP2 的负调控来发挥作用。本研究的结果突出了 PC 治疗的潜在生物标志物。它通过针对 FOXP3 对 SCP2 的负调控来发挥作用。本研究的结果突出了 PC 治疗的潜在生物标志物。它通过针对 FOXP3 对 SCP2 的负调控来发挥作用。本研究的结果突出了 PC 治疗的潜在生物标志物。