Circ_0007385 regulates cell proliferation, apoptosis and stemness via targeting miR‐493‐3p/RAB22A axis in non‐small cell lung cancer

Abstract

Abstract Background Non‐small cell lung cancer (NSCLC) is a common cancer in the United States. Previous studies have shown that circular RNAs (circRNAs) can affect NSCLC progression, but its regulatory mechanism is still indistinct. In this study, we unfold the roles of circular RNA_0007385 in NSCLC tissues and cells. Methods Expression levels of circ_0007385, microRNA‐493‐3p (miR‐493‐3p) and Ras‐related protein Rab‐22A (RAB22A) were detected by quantitative real‐time polymerase chain reaction (qRT‐PCR) in NSCLC tissues and cells. Cell proliferation, apoptosis and stemness were examined by cell counting kit 8 (CCK8) assay, 5‐ethynyl‐2′‐deoxyuridine (EdU) assay, flow cytometry analysis and sphere‐formation assay. The interaction between miR‐493‐3p and circ_0007385 or RAB22A was forecasted by bioinformatic analysis and detected by dual‐luciferase reporter assay, RNA immunoprecipitation (RIP) and RNA pulldown assays. In vivo experiments were implemented to verify the effect of circ_0007385 in vivo. Results Expression of circ_0007385 and RAB22A increased, whereas miR‐493‐3p level was decreased in NSCLC tissues in contrast to that in normal tissues. For functional analysis, circ_0007385 deficiency inhibited cell proliferation and stemness, whereas it promoted cell apoptosis in NSCLC cells. Mechanically, circ_0007385 acted as a miR‐493‐3p sponge to modulate RAB22A expression. Moreover, circ_0007385 could regulate the development of NSCLC by sponging miR‐493‐3p to regulate the expression of RAB22A. In addition, circ_0007385 silence also attenuated tumor growth in vivo. Conclusions Circ_0007385 promoted NSCLC progression by sponging miR‐493‐3p to increase RAB22A expression, which also offered an underlying targeted therapy for NSCLC treatment.

Keywords

• circ_0007385
• miR‐493‐3p
• non‐small cell lung cancer
• RAB22A