Long non‐coding RNA deleted in lymphocytic leukaemia 1 promotes hepatocellular carcinoma progression by sponging miR‐133a to regulate IGF‐1R expression

• DOI: 10.1111/jcmm.14384
• Publication Date: 2019-06-17T16:53:07Z
• Authors: Wei Zhang; Songyang Liu; Kai Liu; Yahui Liu
• Keywords: Male; 0303 health sciences; Carcinoma, Hepatocellular; Epithelial-Mesenchymal Transition; Tumor Suppressor Proteins; Liver Neoplasms; Original Articles; Middle Aged; Receptor, IGF Type 1; 3. Good health; Gene Expression Regulation, Neoplastic; MicroRNAs; 03 medical and health sciences; Cell Movement; Cell Line, Tumor; Humans; Female; RNA, Long Noncoding; Cell Proliferation; Signal Transduction

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