scholarly journals High Expression of LINC01420 indicates an unfavorable prognosis and modulates cell migration and invasion in nasopharyngeal carcinoma

2017 ◽  
Vol 8 (1) ◽  
pp. 97-103 ◽  
Author(s):  
Liting Yang ◽  
Yanyan Tang ◽  
Yi He ◽  
Yumin Wang ◽  
Yu Lian ◽  
...  
2016 ◽  
Vol 13 (4) ◽  
pp. 3236-3242 ◽  
Author(s):  
FANGZHENG WANG ◽  
CHUNER JIANG ◽  
QUANQUAN SUN ◽  
FENQIN YAN ◽  
LEI WANG ◽  
...  

2010 ◽  
Vol 294 (2) ◽  
pp. 159-166 ◽  
Author(s):  
Ching Tung Lum ◽  
Xiong Liu ◽  
Raymond Wai-Yin Sun ◽  
Xiang-Ping Li ◽  
Ying Peng ◽  
...  

2018 ◽  
Vol 7 (8) ◽  
pp. 3862-3874 ◽  
Author(s):  
Qian Hu ◽  
Xiao Lin ◽  
Linxiaoxiao Ding ◽  
Yinduo Zeng ◽  
Danmei Pang ◽  
...  

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 559 ◽  
Author(s):  
Yin Zhao ◽  
Yuan Lei ◽  
Shi-Wei He ◽  
Ying-Qin Li ◽  
Ya-Qin Wang ◽  
...  

Epigenetic regulation plays an important role in the development and progression of nasopharyngeal carcinoma (NPC), but the epigenetic mechanisms underlying NPC metastasis remain poorly understood. Here, we demonstrate that hypermethylation of the UCHL1 promoter leads to its downregulation in NPC. Restoration of UCHL1 inhibited the migration and invasion of NPC cells in vitro and in vivo, and knockdown of UCHL1 promoted NPC cell migration and invasion in vitro and in vivo. Importantly, we found that UCHL1 interacts with CTTN, and may function as a ligase promoting CTTN degradation by increasing K48-linked ubiquitination of CTTN. Additionally, restoration of CTTN in NPC cells that overexpressed UCHL1 rescued UCHL1 suppressive effects on NPC cell migration and invasion, which indicated that CTTN is a functional target of UCHL1 in NPC. Our findings revealed that UCHL1 acts as a tumor suppressor gene in NPC and thus provided a novel therapeutic target for NPC treatment.


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