Overexpression of LncRNA ILF3-AS1 restrained NSCLC development through miR-185-5p/ING4 axis

Abstract

Abstract LncRNA ILF3-AS1 was abnormally expressed in several cancers. However, the relationship of ILF3-AS1 and non-small cell lung cancer (NSCLC) still unknown. Now, our research endeavored to characterize the expression and function of ILF3-AS1 in NSCLC, so as to study its related mechanism. The differential level of ILF3-AS1 in NSCLC were detected. The relation of miR-185-5p with ILF3-AS1 and ING4 was predicted by bioinformatics online tool and further verified. The influence of ILF3-AS1 and miR-185-5p inhibitor on cell biological function were detected by a series of tests. The changes of tumor volume and weight intervened by ILF3-AS1 up-regulation and miR-185-5p depletion were monitored in mice. ILF3-AS1 was abnormally down-expressed not only in NSCLC tissues, but also in NSCLC cells. ILF3-AS1 overexpression can inhibit the viability of NSCLC cells, reduce the number of migrating and invading cells, and enhance the apoptosis, which was reversed by miR-185-5p mimics. There were direct interactions between miR-185-5p, ILF3-AS1, and ING4. Tumor inhibition was observed in mice transplanted with H1299 transfected by pcDNA3.1-ILF3-AS1 and miR-185-5p inhibitor. ILF3-AS1 modulated NSCLC progress through targeting miR-185-5p/ING4 axis.