AF119895 regulates NXF3 expression to promote migration and invasion of hepatocellular carcinoma through an interaction with miR-6508-3p

AF119895 regulates NXF3 expression to promote migration and invasion of hepatocellular carcinoma... Various studies revealed that numerous long noncoding RNAs (lncRNAs) have been found dysregulated in HCC and played important role in hepatocarcinogenesis, although the underlying mechanism still remains unclear. Herein, we reported AF119895, a new lncRNA which was identified from microarray and amplified in HCC. Functionally, AF119895 promoted migration and invasion of HCC cells both in vitro and in vivo. Furthermore, we identified that NXF3 was a downstream target of AF119895. NXF3 depletion could decrease HCC cells migration and invasion. In addition, AF119895 could act as an endogenous sponge by binding to miR-6508-3p and reduce miR-6508-3p expression. And miR-6508-3p could regulate NXF3 by interacting with its 3′UTR. These observations collectively demonstrate that AF119895 modulates the repression of NXF3 by binding to miR-6508-3p. Our results outline a novel signaling pathway mediated by AF119895 and suggest its candidacy as a new prognostic biomarker and therapeutic target of HCC. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Experimental Cell Research Elsevier

AF119895 regulates NXF3 expression to promote migration and invasion of hepatocellular carcinoma through an interaction with miR-6508-3p

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Publisher
Elsevier
Copyright
Copyright © 2017 Elsevier Inc.
ISSN
0014-4827
D.O.I.
10.1016/j.yexcr.2017.12.016
Publisher site
See Article on Publisher Site

Abstract

Various studies revealed that numerous long noncoding RNAs (lncRNAs) have been found dysregulated in HCC and played important role in hepatocarcinogenesis, although the underlying mechanism still remains unclear. Herein, we reported AF119895, a new lncRNA which was identified from microarray and amplified in HCC. Functionally, AF119895 promoted migration and invasion of HCC cells both in vitro and in vivo. Furthermore, we identified that NXF3 was a downstream target of AF119895. NXF3 depletion could decrease HCC cells migration and invasion. In addition, AF119895 could act as an endogenous sponge by binding to miR-6508-3p and reduce miR-6508-3p expression. And miR-6508-3p could regulate NXF3 by interacting with its 3′UTR. These observations collectively demonstrate that AF119895 modulates the repression of NXF3 by binding to miR-6508-3p. Our results outline a novel signaling pathway mediated by AF119895 and suggest its candidacy as a new prognostic biomarker and therapeutic target of HCC.

Journal

Experimental Cell ResearchElsevier

Published: Feb 1, 2018

References

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