Long non-coding RNA (lncRNA) has been demonstrated as vital regulator in human cancer. However, the precise role of lnc-TDRG1 in cervical cancer (CC) remains unclear, so this study was aimed to clarify the role and underlying molecular mechanism of lnc-TDRG1 in CC. The real-time quantitative polymerase chain reaction (RT-qPCR) was conducted to assess the expression levels of lnc-TDRG1, miR-214-5p and Semaphorin 4C (SEMA4C). Under hypoxia condition, the biological behaviors of CC cell, including invasion and glycolysis were determined by transwell assay and Glucose Assay Kit and Lactate Assay Kit, respectively. The Western blot assay was employed to test the expression level of SEMA4C and hexokinase 2 (HK2) expression. The interaction relationship between miR-214-5p and lnc-TDRG1 or SEMA4C was analyzed bioinformatics database and confirmed by dual-luciferase reporter assay, respectively. A xenograft experiment in nude mice was established to clarify the functional role of lnc-TDRG1 in vivo. We found Lnc-TDRG1 was highly expressed in CC tissues and cells and it was upregulated in response to hypoxia. Loss-of-functional experiment suggested that knockdown of lnc-TDRG1 impede invasion, hypoxia-induced glycolysis in vitro and tumor growth in vivo, which was abolished by knockdown of miR-214-5p or overexpression of SEMA4C. Moreover, we confirmed that miR-214-5p specifically bound to SEMA4C and negatively correlated with SEMA4C expression. Collectively, lnc-TDRG1 regulated SEMA4C expression by sponging miR-214-5p in CC. Collectively, mechanistically, lnc-TDRG1 could act as a sponge of miR-214-5p to regulate the expression of SEMA4C, and further regulate invasion and hypoxia-glycolysis in CC cells.

长链非编码 RNA (lncRNA) 已被证明是人类癌症的重要调节因子。然而，lnc-TDRG1在宫颈癌（CC）中的确切作用尚不清楚，因此本研究旨在阐明lnc-TDRG1在宫颈癌中的作用和潜在分子机制。进行实时定量聚合酶链反应 (RT-qPCR) 以评估 lnc-TDRG1、miR-214-5p 和信号素 4C (SEMA4C) 的表达水平。缺氧条件下，分别采用transwell实验、葡萄糖检测试剂盒和乳酸检测试剂盒检测CC细胞的侵袭和糖酵解等生物学行为。使用蛋白质印迹测定来测试 SEMA4C 和己糖激酶 2 (HK2) 表达的表达水平。miR-214-5p 与 lnc-TDRG1 或 SEMA4C 之间的相互作用关系通过生物信息学数据库进行分析，并分别通过双荧光素酶报告基因测定证实。建立裸鼠异种移植实验以阐明lnc-TDRG1在体内的功能作用。我们发现 Lnc-TDRG1 在 CC 组织和细胞中高表达，并且在缺氧时上调。功能丧失实验表明，lnc-TDRG1 的敲低阻碍了侵袭、体外缺氧诱导的糖酵解和体内肿瘤的生长，这被 miR-214-5p 的敲低或 SEMA4C 的过表达所消除。此外，我们证实 miR-214-5p 与 SEMA4C 特异性结合并与 SEMA4C 表达呈负相关。总的来说，lnc-TDRG1 通过在 CC 中海绵 miR-214-5p 来调节 SEMA4C 表达。总的来说，机械地，