Abstract
Long non-coding RNA (lncRNA) deleted in lymphocytic leukaemia 1 (DLEU1) was reported to be involved in the occurrence and development of multiple cancers. However, the exact expression, biological function and underlying mechanism of DLEU1 in hepatocellular carcinoma (HCC) remain unclear. In this study, real-time quantitative polymerase chain reaction (qRT-PCR) in HCC tissues and cell lines revealed that DLEU1 expression was up-regulated, and the increased DLEU1 was closely associated with advanced tumour-node-metastasis stage, vascular metastasis and poor overall survival. Function experiments showed that knockdown of DLEU1 significantly inhibited HCC cell proliferation, colony formation, migration and invasion, and suppressed epithelial to mesenchymal transition (EMT) process via increasing the expression of E-cadherin and decreasing the expression of N-cadherin and Vimentin. Luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay demonstrated that DLEU1 could sponge miR-133a. Moreover, miR-133a inhibition significantly reversed the suppression effects of DLEU1 knockdown on HCC cells. Besides, we found that silenced DLEU1 significantly decreased insulin-like growth factor 1 receptor (IGF-1R) expression (a target of miR-133a) and its downstream signal PI3K/AKT pathway in HCC cells, while miR-133a inhibitor partially reversed this trend. Furthermore, DLEU1 knockdown impaired tumour growth in vivo by regulating miR-133a/IGF-1R axis. Collectively, these findings indicate that DLEU1 promoted HCC progression by sponging miR-133a to regulate IGF-1R expression. Deleted in lymphocytic leukaemia 1/miR-133a/IGF-1R axis may be a novel target for treatment of HCC.