LAUSR

Many studies have shown that circular RNA (circRNA) is an important regulator mediating the malignant progression of cancer. However, the role and mechanism of circ‐EIF3I in lung cancer (LC) development are still unclear. A total 36 paired LC tumor tissues and adjacent normal tissues were enrolled. The expression of circ‐EIF3I, microRNA (miR)‐1253, and neuro‐oncological ventral antigen 2 (NOVA2) was measured by quantitative real‐time PCR. The proliferation, apoptosis, migration, and invasion of LC cells were determined by MTT assay, colony formation assay, flow cytometry, and transwell assay. Dual‐luciferase reporter assay was performed to verify the interaction between miR‐1253 and circ‐EIF3I or NOVA2. The protein levels of NOVA2 and Wnt/β‐catenin pathway‐related markers were detected by western blot analysis. Xenograft tumor was constructed to explore the function of circ‐EIF3I on LC tumor growth. Circ‐EIF3I was upregulated in LC tumor tissues and cells. Silenced circ‐EIF3I could suppress the proliferation, migration, invasion, and enhance the apoptosis of LC cells in vitro, as well as reduce LC tumor growth in vivo. Circ‐EIF3I could sponge miR‐1253, and miR‐1253 inhibitor overturned the regulation of circ‐EIF3I knockdown on LC cell progression. NOVA2 was confirmed to be a target of miR‐1253, which could reverse the inhibitory effects of miR‐1253 on LC cell progression. Further experiments showed that circ‐EIF3I regulated NOVA2 expression by sponging miR‐1253. In addition, circ‐EIF3I silencing could inhibit the activity of Wnt/β‐catenin pathway via regulating the miR‐1253/NOVA2 axis. Circ‐EIF3I might function as an oncogene in LC, which promoted LC progression by the miR‐1253/NOVA2/Wnt/β‐catenin network.