LINC00342 regulates the PI3K-AKT signaling pathway via the miR-149-5p/FGF11 axis and affects the progression of oral cancer

Abstract

Background A large amount of long non-coding RNAs (lncRNAs) have been demonstrated to be involved in the progression of oral cancer (OC). The purpose of this study was to investigate the role of a novel lncRNA, LINC00342, in OC and its molecular mechanism. Methods and results In this study, differentially expressed LncRNA/miRNA/mRNAs were analyzed by Gene Expression Omnibus database, and their expression levels and effects on cell viability and cell cycle in OC cells were detected by RT-qPCR and Cell Counting Kit-8 and flow cytometry. The binding between RNAs was analyzed by dual luciferase, and western blot was used to detect the activation of relevant pathways. Our study showed that, in contrast to miR-149-5p, the expression of LINC00342 and fibroblast growth factor 11 (FGF11) were upregulated in OC cells, and dual-luciferase assays confirmed that they bind to miR-149-5p in a direct targeting manner. In addition, inhibition of LINC00342 expression resulted in decreased proliferation rate and migration ability of OC cells, cell cycle arrest in G1 phase, and inhibition of PI3K-AKT signaling. And inhibition of miR-149-5p or overexpression of FGF11 reversed the effects of si-LINC00342. Conclusions LINC00342 promotes PI3K-AKT signaling by activating FGF11 through adsorption of miR-149-5p, thereby regulating the progression of OC.