scholarly journals p53‐inducible gene 3 promotes cell migration and invasion by activating the FAK /Src pathway in lung adenocarcinoma

2018 ◽  
Vol 109 (12) ◽  
pp. 3783-3793 ◽  
Author(s):  
Meng‐Meng Gu ◽  
Dexuan Gao ◽  
Ping‐An Yao ◽  
Lan Yu ◽  
Xiao‐Dong Yang ◽  
...  
2021 ◽  
Vol 567 ◽  
pp. 222-229
Author(s):  
Yiliang Meng ◽  
Liu Yang ◽  
Xiao Wei ◽  
Hongcheng Luo ◽  
Yingying Hu ◽  
...  

2018 ◽  
Vol 497 (2) ◽  
pp. 633-638 ◽  
Author(s):  
Xueying Li ◽  
Jiaqi Jin ◽  
Siyuan Yang ◽  
Weizhi Xu ◽  
Xianbin Meng ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Jiaqian Xu ◽  
Haoyan Guo ◽  
Zhengcao Xing ◽  
Wenlong Zhang ◽  
Jianli He ◽  
...  

Nuclear factor erythroid 2-related factor 2 (NRF2) is a crucial transcription factor for cell adaptation and defense against oxidative stress. NRF2 activation confers Kras/Lkb1/Keap1 (KLK) mutant tumor cells with greater resistance to oxidative insults. We previously reported that SUMOylation at lysine residue 110 is important for the ability of NRF2 to promote reactive oxygen species (ROS) clearance in hepatocellular carcinoma. In this study, we investigated whether SUMOylation is necessary for the ability of NRF2 to inhibit KLK lung adenocarcinoma (LUAD) cell migration and invasion. Our experiments showed that mild oxidative stress reduced NRF2 SUMOylation, which promoted KLK LUAD cell migration and invasion. Mechanistically, NRF2 SUMOylation increased the antioxidant ability of NRF2 and reduced cellular ROS levels, mainly by transcriptionally activating Cat in KLK LUAD cells. With reduced NRF2 SUMOylation, increased ROS acted as signaling molecules to activate the JNK/c-Jun axis, which enhanced cell mobility and cell adhesion, to promote LUAD cell migration and invasion. Taken together, the results of this study reveal a novel signaling process in which reduced NRF2 SUMOylation permits increased KLK LUAD cell migration and invasion under mild oxidative stress.


Cell Cycle ◽  
2019 ◽  
Vol 18 (21) ◽  
pp. 2972-2985 ◽  
Author(s):  
Guodong Xiao ◽  
Peili Wang ◽  
Xiaoqiang Zheng ◽  
Dapeng Liu ◽  
Xin Sun

2020 ◽  
Vol 11 (11) ◽  
Author(s):  
Xiangying Deng ◽  
Wei Xiong ◽  
Xianjie Jiang ◽  
Shanshan Zhang ◽  
Zheng Li ◽  
...  

Abstract There is increasing evidence that long non-coding RNAs (lncRNAs) play important roles in human tumorigenesis. By using publicly available expression profiling data from lung adenocarcinoma and integrating bioinformatics analysis, we screened a lncRNA, LINC00472. LINC00472 expression in lung adenocarcinoma tissues was significantly lower and tightly associated with patient prognosis and TNM clinical stages in lung adenocarcinoma. LINC00472 also inhibited lung adenocarcinoma cell migration and invasion and increased cell stiffness and adhesion. RNA pull down and RIP assays identified that LINC00472 interacted with the transcription factor Y-box binding protein 1 (YBX1), which partially reversed the inhibition of cell migration and invasion and increased LINC00472-induced cell stiffness and adhesion. LINC00472 also regulated the density and integrity of F-actin in A549 and PC-9 cells possibly via YBX1. LINC00472 inhibited the cell epithelial-mesenchymal transition (EMT) processes via the modulation of YBX1. These results indicated that LINC00472 inhibited the cell EMT process by binding to YBX1, and affected the mechanical properties of the cell, ultimately inhibited its ability to invade and metastasize. Collectively, the present study provides the first evidence that LINC00472 changes the mechanical properties and inhibits the invasion and metastasis of lung adenocarcinoma cells.


Sign in / Sign up

Export Citation Format

Share Document