Generation of a Potential Prognostic Matrix for Papillary Thyroid Cancer that Assesses Age, Tumor Size, Transforming Growth Factor-β, and BRAFV600E Mutation

2017 ◽  
Vol 40 (10) ◽  
pp. 586-592
Author(s):  
Ping Wang ◽  
Yu Lun ◽  
Yudong Fu ◽  
Fei Wang ◽  
Shihua Zhao ◽  
...  
2020 ◽  
Vol 295 (31) ◽  
pp. 10726-10740
Author(s):  
Hongwei Gao ◽  
Peirong Bai ◽  
Lin Xiao ◽  
Mengjia Shen ◽  
Qiuxiao Yu ◽  
...  

Mediator complex subunit 16 (MED16) is a component of the mediator complex and functions as a coactivator in transcriptional events at almost all RNA polymerase II–dependent genes. In this study, we report that the expression of MED16 is markedly decreased in papillary thyroid cancer (PTC) tumors compared with normal thyroid tissues. In vitro, MED16 overexpression in PTC cells significantly inhibited cell migration, enhanced sodium/iodide symporter expression and iodine uptake, and decreased resistance to radioactive 131I (RAI). Conversely, PTC cells in which MED16 had been further knocked down (MED16KD) exhibited enhanced cell migration, epithelial–mesenchymal transition, and RAI resistance, accompanied by decreased sodium/iodide symporter levels. Moreover, cell signaling through transforming growth factor β (TGF-β) was highly activated after the MED16 knockdown. Similar results were obtained in MED12KD PTC cells, and a co-immunoprecipitation experiment verified interactions between MED16 and MED12 and between MED16 and TGF-βR2. Of note, the application of LY2157299, a potent inhibitor of TGF-β signaling, significantly attenuated MED16KD-induced RAI resistance both in vitro and in vivo. In conclusion, our findings indicate that MED16 reduction in PTC contributes to tumor progression and RAI resistance via the activation of the TGF-β pathway.


2016 ◽  
Vol 31 (3) ◽  
pp. 397 ◽  
Author(s):  
Eon Ju Jeon ◽  
Young Ju Jeong ◽  
Sung Hwan Park ◽  
Chang Ho Cho ◽  
Ho Sang Shon ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document