Long non-coding RNAs PGM5-AS1 upregulates Decorin (DCN) to inhibit cervical cancer progression by sponging miR-4284

Long non-coding RNAs (lncRNAs) have been widely studied and play crucial roles in cervical cancer (CC) progression. Here, we investigated the function and mechanism of lncRNA PGM5-AS1 action in CC cells. Using real-time quantitative polymerase chain reaction or western blotting, PGM5-AS1 and decorin (DCN) were downregulated in CC tissues and cells, whereas miR-4284 was upregulated. Luciferase assay, RNA pull-down assay, and western blotting showed that PGM5-AS1 could sponge miR-4284 to upregulate DCN expression in CC cells. Additionally, cell functional experiments showed that PGM5-AS1 overexpression led to decreased proliferation, migration, and invasion of CC cells. However, the inhibitory effect of PGM5-AS1 overexpression on CC cells was partly relieved by DCN knockdown because of the targeting interaction between PGM5-AS1, miR-4284, and DCN. In summary, this study identified that PGM5-AS1 negatively regulates CC cell malignancy by targeting miR-4284/DCN.

长链非编码RNA（long non-coding RNAs，lncRNAs）已被广泛研究，并在宫颈癌（cervical cancer，CC）的发生发展中发挥关键作用。本研究旨在探讨长链非编码RNA PGM5-AS1在宫颈癌细胞中的功能及其作用机制。通过实时定量聚合酶链反应与蛋白质印迹法检测发现，PGM5-AS1与核心蛋白聚糖（decorin，DCN）在宫颈癌组织及宫颈癌细胞中均呈低表达，而miR-4284则呈高表达。荧光素酶报告基因实验、RNA pull-down实验及蛋白质印迹法结果证实，PGM5-AS1可通过海绵吸附作用靶向结合miR-4284，从而上调宫颈癌细胞中DCN的表达水平。此外，细胞功能实验结果显示，过表达PGM5-AS1可显著抑制宫颈癌细胞的增殖、迁移与侵袭能力。但由于PGM5-AS1、miR-4284与DCN三者间存在靶向调控关系，敲低DCN可部分逆转过表达PGM5-AS1对宫颈癌细胞的增殖抑制效应。综上，本研究证实PGM5-AS1可通过靶向调控miR-4284/DCN轴，负向调控宫颈癌细胞的恶性表型。