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Basic Information

Classification Information

Regulatory Mechanism		Biological Function		Clinical Application
TF		Immune		Survival
Enhancer		Apoptosis		Drug
Variant		Cell Growth		Circulating
MiRNA		EMT		Metastasis
Methylation		Coding Ability		Recurrence

Cancer&Entry Information

Cancer Name	hepatocellular carcinoma
ICD-0-3	C22.0
Methods	qPCR, Western blot, Luciferase reporter assay, RIP
Sample	HCC cell lines (SMMC-7721, Hep3B, HepG2, Huh-7) and normal hepatic epithelial cell line LO2, HCC tissues and paired adjacent tissues
Expression Pattern	up-regulated
Function Description	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 inva- sion, and suppressed epithelial to mesenchymal transition (EMT) process via increas- ing 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 sig- nal PI3K/AKT pathway in HCC cells, while miR-133a inhibitor partially reversed this trend. Furthermore, DLEU1 knockdown impaired tumour growth in vivo by regulat- ing miR-133a/IGF-1R axis.
Pubmed ID	31207081
Year	2019
Title	Long non-coding RNA deleted in lymphocytic leukaemia 1 promotes hepatocellular carcinoma progression by sponging miR-133a to regulate IGF-1R expression

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