Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.febslet.2011.05.042
Title: MiR-198 inhibits migration and invasion of hepatocellular carcinoma cells by targeting the HGF/c-MET pathway
Authors: Tan, S.
Li, R.
Ding, K.
Lobie, P.E. 
Zhu, T.
Keywords: c-MET
Hepatocellular carcinoma
Invasion
miR-198
Issue Date: 21-Jul-2011
Citation: Tan, S., Li, R., Ding, K., Lobie, P.E., Zhu, T. (2011-07-21). MiR-198 inhibits migration and invasion of hepatocellular carcinoma cells by targeting the HGF/c-MET pathway. FEBS Letters 585 (14) : 2229-2234. ScholarBank@NUS Repository. https://doi.org/10.1016/j.febslet.2011.05.042
Abstract: Metastasis is the leading cause of death in patients with hepatocellular carcinoma (HCC) and microRNAs have been implicated to influence this process. Emerging evidence indicates that miR-198 is down-regulated in HCC compared to normal liver parenchyma, but the functional roles of miR-198 in HCC cells remains unexplored. Herein, we show that miR-198 directly targets c-MET via its 3′UTR. Forced expression of miR-198 decreased c-MET expression at both mRNA and protein levels and consequently diminished HGF induced phosphorylation of p44/42 MAPK in HCC cells. Forced expression of miR-198 inhibited HGF promotion of HCC cell migration and invasion in a c-MET dependent manner. In conclusion, we have identified miR-198 as a novel suppressor of HCC cell invasion by negative regulation of the HGF/c-MET pathway. © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Source Title: FEBS Letters
URI: http://scholarbank.nus.edu.sg/handle/10635/109468
ISSN: 00145793
DOI: 10.1016/j.febslet.2011.05.042
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.

SCOPUSTM   
Citations

96
checked on Jan 30, 2023

WEB OF SCIENCETM
Citations

92
checked on Jan 30, 2023

Page view(s)

151
checked on Jan 26, 2023

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.