Circular RNA_0001073 (circ_0001073) Suppresses The Progression of Non-Small Cell Lung Cancer via miR-582-3p/RGMB Axis (Pages: 684-691)


Xuefen Jing , Meiying Ren , Yongshun Fan , Yuhua Fu , Cuifeng Wang *,

Objective

Reportedly, circular RNAs (circRNAs) exert a crucial regulatory role in cancer. Circ_0001073 is derived from exons 3-5 of ACVR2A gene, which inhibits cancer progression. However, the role and mechanism of circ_0001073 in non-small cell lung cancer (NSCLC) are unclear. This study aimed to explore the role and mechanism of circ_0001073 in the development of NSCLC.

MaterialsAndMethods

In this experimental study, microarray analysis was employed to filter differential expressed circRNAs in NSCLC tissues. Also, circ_0001073, microRNA-582-3p (miR-582-3p), and repulsive guidance molecule B (RGMB) mRNA expressions were examined by quantitative real-time polymerase chain reaction (qRT-PCR). NSCLC cell multiplication was measured by the cell counting kit-8 (CCK-8) assay. Scratch healing experiment and Transwell experiment were performed to assess cell migration and invasion, respectively. Flow cytometry was applied to analyze the apoptosis of NSCLC cells. Western blot was employed to assess RGMB protein expression. Additionally, dualluciferase reporter gene experiment and RNA immunoprecipitation (RIP) experiment were applied to probe the binding sites between miR-582-3p and circ_0001073 or RGMB..

Results

Circ_0001073 was remarkably under-expressed in NSCLC tissues and cells. Circ_0001073 overexpression impeded the multiplication, migration, and invasion and enhanced the apoptosis of NSCLC cells in vitro. Circ_0001073 directly bound to miR-582-3p and acted as a miRNA sponge to regulate RGMB expression. Besides, miR-582-3p overexpression or knockdown of RGMB remarkably reversed the malignant phenotypes of NSCLC cells induced by the up-regulation of circ_0001073 expression.

Conclusion

Circ_0001073 up-regulates RGMB expression through adsorbing miR-582-3p to inhibit NSCLC progression, suggesting its potential as a novel therapeutic target in NSCLC.