Long noncoding RNA (lncRNA), a subgroup of noncoding RNA with > 200 nt, plays critical roles in cancer progression. Here, we aimed to explore the detailed biological function of lncRNA EGFEM1P during papillary thyroid cancer (PTC) progression. RT-qPCR and Western blot were used to analyze the expression of lncRNA EGFEM1P, miR-6867-5p, and CHI3L1. CCK8, colony formation, and Transwell migration assays were undertaken to assess PTC cell proliferation and migration. A xenograft tumor mouse model was also used to establish tumor growth in vivo. Luciferase reporter and anti-AGO2 RNA immunoprecipitation (RIP) assays were used to clarify the interplay between miR-6867-5p and lncRNA EGFEM1P or CHI3L1. We found lncRNA EGFEM1P and CHI3L1 to be highly expressed in PTC tissues and cells, while miR-6867-5p expression decreases. Functionally, lncRNA EGFEM1P silence delays PTC cell proliferation and migration, and impairs tumorigenesis in vivo. LncRNA EGFEM1P targets miR-6867-5p, and CHI3L1 is a target gene of miR-6867-5p. LncRNA EGFEM1P silence decreases the pro-proliferation and pro-migration caused by the miR-6867-5p inhibitor in PTC cells, and CHI3L1 silence abrogates the pro-tumorigenic action resulting from the miR-6867-5p inhibitor in PTC cells. Our data showed that lncRNA EGFEM1P targeting of the miR-6867-5p/CHI3L1 axis drives PTC progression, suggesting lncRNA EGFEM1P as a therapeutically target for PTC.

中文翻译：

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lncRNA EGFEM1P 通过调节 miR-6867-5p/CHI3L1 轴驱动乳头状甲状腺癌的进展

长非编码 RNA (lncRNA) 是长度大于 200 nt 的非编码 RNA 亚群，在癌症进展中发挥着关键作用。在这里，我们的目的是探讨lncRNA EGFEM1P在甲状腺乳头状癌（PTC）进展过程中的详细生物学功能。采用RT-qPCR和Western blot分析lncRNA EGFEM1P、miR-6867-5p和CHI3L1的表达。采用 CCK8、集落形成和 Transwell 迁移测定来评估 PTC 细胞增殖和迁移。还使用异种移植肿瘤小鼠模型来建立体内肿瘤生长。使用荧光素酶报告基因和抗 AGO2 RNA 免疫沉淀 (RIP) 测定来阐明 miR-6867-5p 和 lncRNA EGFEM1P 或 CHI3L1 之间的相互作用。我们发现lncRNA EGFEM1P和CHI3L1在PTC组织和细胞中高表达，而miR-6867-5p表达下降。从功能上讲，lncRNA EGFEM1P 沉默会延迟 PTC 细胞增殖和迁移，并损害体内肿瘤发生。LncRNA EGFEM1P 靶向 miR-6867-5p，CHI3L1 是 miR-6867-5p 的靶基因。LncRNA EGFEM1P 沉默降低了 PTC 细胞中 miR-6867-5p 抑制剂引起的促增殖和促迁移，CHI3L1 沉默消除了 PTC 细胞中 miR-6867-5p 抑制剂引起的促肿瘤作用。我们的数据显示，靶向 miR-6867-5p/CHI3L1 轴的 lncRNA EGFEM1P 驱动 PTC 进展，表明 lncRNA EGFEM1P 作为 PTC 的治疗靶点。