Long non-coding RNA LINP1 induces tumorigenesis of Wilms' tumor by affecting Wnt/β-catenin signaling pathway.

Abstract

Recent studies have discovered that long non-coding RNAs (lncRNAs) play an important role in the development of malignant tumors. The aim of this work was to investigate the exact role of lncRNA LINP1 in the development of Wilms' tumor and to explore the possible underlying mechanism. The expression of lncRNA in non-homologous end joining pathway 1 (LINP1) in tissue samples of Wilms' tumor was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). The relationship between the expression of lung cancer associated transcript 1 (LUCAT1) and patients' overall survival time was analyzed. Subsequent functional experiments were conducted to identify the changes in biological behaviors of Wilms' tumor cells after the gain or loss of LINP1. Moreover, the underlying mechanism of LINP1 function was explored. QRT-PCR results showed that LINP1 expression level in Wilms' tumor tissues was significantly higher than that of adjacent tissues. LINP1 expression was negatively associated with the overall survival time of patients with Wilms' tumor. Cell growth ability was markedly inhibited and promoted after down-regulation and overexpression of LINP1 in vitro, respectively. Moreover, after the loss and gain of LINP1 in vitro, cell migration and invasion abilities were remarkably repressed and promoted, respectively. Furthermore, the loss of LINP1 in vitro could significantly decrease the expressions of targeted proteins in the Wnt/β-catenin signaling pathway. However, the expressions of targeted proteins in the Wnt/β-catenin signaling pathway were remarkably up-regulated after over-expression of LINP1. LINP1 could enhance cell metastasis and proliferation via inducing the Wnt/β-catenin signaling pathway. Our findings might provide a new prospect for the diagnosis and therapy of Wilms' tumor.