Maternal embryonic leucine zipper kinase serves as a potential prognostic marker and leads to sorafenib chemoresistance modified by miR-142-5p in hepatocellular carcinoma

Author(s):  
Hualei Li ◽  
Ling Gai ◽  
Zhimei Wu ◽  
Feng Li
2016 ◽  
Vol 46 (9) ◽  
pp. 916-923 ◽  
Author(s):  
Chihiro Dohi ◽  
Kazuhiro Nouso ◽  
Koji Miyahara ◽  
Yuki Morimoto ◽  
Nozomu Wada ◽  
...  

Oncotarget ◽  
2016 ◽  
Vol 7 (35) ◽  
pp. 56798-56810 ◽  
Author(s):  
Kun Liu ◽  
Yuening Zhang ◽  
Chengdong Zhang ◽  
Qinle Zhang ◽  
Jiatong Li ◽  
...  

2016 ◽  
Vol 15 (3) ◽  
Author(s):  
C.W. Dong ◽  
Y.X. Wang ◽  
F.T. Du ◽  
W. Ding ◽  
S.Y. Hu

Author(s):  
Minhua Wu ◽  
Xubin Deng ◽  
Yu Zhong ◽  
Li Hu ◽  
Xiujuan Zhang ◽  
...  

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.


Sign in / Sign up

Export Citation Format

Share Document