LncRNA TDRG1 promotes the proliferation, migration, and invasion of cervical cancer cells by sponging miR-214-5p to target SOX4

SOX4型 癌症研究 转染 免疫印迹 报告基因 细胞生长 实时聚合酶链反应 生物 细胞迁移 细胞 细胞生物学 细胞培养 分子生物学 基因表达 基因 发起人 遗传学
作者
Meijun Guo,Beibei Lin,Guoping Li,Jizhen Lin,Xingxing Jiang
出处
期刊:Journal of Receptors and Signal Transduction [Informa]
卷期号:40 (3): 281-293 被引量:16
标识
DOI:10.1080/10799893.2020.1731537
摘要

The pathogenesis of cervical cancer (CC) at molecular level has attracted much research attention. The current study aimed to explore the effects of LncRNA TDRG1 on cellular process in CC cells and its molecular mechanism. Expressions of TDRG1 and miR-214-5p in CC and normal tissues and CC cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The effects of TDRG1, miR-214-5p, and SOX4 on cell proliferation, migration, invasion, and EMT process of CC cells were detected by Cell Counting Kit-8 (CCK-8), colony formation, wound-healing, Transwell, and Western blot assays, respectively. StarBase and Targetscan7.2 were used to predict the target genes of TDRG1 and miR-214-5p, and the predictions were verified by dual-luciferase reporter assay. The expression of SOX4 in CC and normal tissues, and CC cells transfected with siTDRG1 or miR-214-5p inhibitor was determined by qRT-PCR. The results showed that expression of TDRG1 was up-regulated, while that of miR-214-5p was down-regulated in CC. The target genes of TDRG1 and miR-214-5p were verified to be miR-214-5p and SOX4, respectively. Knocking down TDRG1 expression could inhibit cell proliferation, colony, migration, and invasion abilities, and EMT process, whereas the inhibition of miR-214-5p expression partially reversed such results. Moreover, high SOX4 expression was observed in CC tissues, and down-regulating TDRG1 expression reduced the SOX4 expression while down-regulating miR-214-5p expression alleviated such an inhibition. In conclusion, TDRG1 acts as cancer promoter in CC through promoting cell proliferation, migration, invasion, and EMT process to modulate SOX4 expression through adsorbing miR-214-5p.

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