Long non-coding RNA unigene56159 promotes epithelial-mesenchymal transition by acting as a ceRNA of miR-140-5p in hepatocellular carcinoma cells

Highlights • Long non-coding RNA Unigene56159 expression is induced by HBV. • Unigene56159 promotes cell migration/invasion and EMT in HCC. • Unigene56159 functions as a ceRNA for miR-140-5p to de-repress the Slug expression. • The Unigene56159/miR-140-5p/Slug axis contributes to HCC cell migration...

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Bibliographic Details
Published in:Cancer letters 2016-11, Vol.382 (2), p.166-175
Main Authors: Lv, Jing, Fan, Hong-xia, Zhao, Xiao-pei, Lv, Ping, Fan, Jing-yi, Zhang, Yi, Liu, Min, Tang, Hua
Format: Article
Language:English
Subjects:
Apoptosis
Carcinoma, Hepatocellular - genetics
Carcinoma, Hepatocellular - metabolism
Carcinoma, Hepatocellular - pathology
Carcinoma, Hepatocellular - virology
Cell growth
Cell Movement
Cell Transformation, Viral
Cloning
Conflicts of interest
Epithelial-Mesenchymal Transition
Gene expression
Gene Expression Regulation, Neoplastic
HCC migration/invasion
Hematology, Oncology and Palliative Medicine
Hep G2 Cells
Hepatitis
Hepatitis B - complications
Hepatitis B virus
Hepatitis B virus - pathogenicity
Host-Pathogen Interactions
Humans
Liver cancer
Liver Neoplasms - genetics
Liver Neoplasms - metabolism
Liver Neoplasms - pathology
Liver Neoplasms - virology
lncRNA-Unigene56159
Long non-coding RNA (lncRNA)
Metastasis
MicroRNAs - genetics
MicroRNAs - metabolism
miR-140-5p
Mutation
Neoplasm Invasiveness
Plasmids
Proteins
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
Signal Transduction
Slug
Snail Family Transcription Factors - genetics
Snail Family Transcription Factors - metabolism
Transfection
Tumorigenesis
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Description
Summary:Highlights • Long non-coding RNA Unigene56159 expression is induced by HBV. • Unigene56159 promotes cell migration/invasion and EMT in HCC. • Unigene56159 functions as a ceRNA for miR-140-5p to de-repress the Slug expression. • The Unigene56159/miR-140-5p/Slug axis contributes to HCC cell migration and invasion.
ISSN:0304-3835
1872-7980
DOI:10.1016/j.canlet.2016.08.029