@Article{096504020X15796890809840,
AUTHOR = {Minhua Wu, Xubin Deng, Yu Zhong, Li Hu, Xiujuan Zhang, Yanqin Liang, Xiaofang Li, Xiaoxia Ye},
TITLE = {MafF Is Regulated via the circ-ITCH/miR-224-5p Axis and Acts  as a Tumor Suppressor in Hepatocellular Carcinoma},
JOURNAL = {Oncology Research},
VOLUME = {28},
YEAR = {2020},
NUMBER = {3},
PAGES = {299--309},
URL = {http://www.techscience.com/or/v28n3/48533},
ISSN = {1555-3906},
ABSTRACT = {MafF is a member of the basic leucine zipper (bZIP) transcription factor Maf family and is commonly 
downregulated in multiple cancers. But the expression and function of MafF in hepatocellular carcinoma 
(HCC) remain unclear. In this study, we investigated the relationship between endogenous MafF expression 
and HCC progression and explored the regulatory mechanism of MafF expression in HCC. We found that MafF 
decreased in HCC tissues and cells. Lentivirus-mediated MafF overexpression inhibited HCC cell proliferation 
and induced cell apoptosis. Bioinformatics analysis and luciferase assay identified MafF as a direct target of 
miR-224-5p. RNA pull-down assay demonstrated that circular RNA circ-ITCH could sponge miR-224-5p specifically in HCC. The rescue experiments further elucidated that the expression and antitumor effects of MafF 
could be regulated via the circ-ITCH/miR-224-5p axis. This study verified that MafF acted as a tumor suppressor in HCC and revealed the upstream regulation mechanism of MafF, which provided a new perspective for 
potential therapeutic targets of HCC.},
DOI = {10.3727/096504020X15796890809840}
}