miR‐206 inhibits thyroid cancer proliferation and invasion by targeting RAP1B

2019 ◽  
Vol 120 (11) ◽  
pp. 18927-18936 ◽  
Author(s):  
Peng Wang ◽  
Jialei Gu ◽  
Kejing Wang ◽  
Jinbiao Shang ◽  
Wendong Wang
2017 ◽  
Vol 50 (5) ◽  
pp. 1567-1578 ◽  
Author(s):  
Jing Zhong ◽  
Chang Liu ◽  
Qing Hai Zhang ◽  
Ling Chen ◽  
Ying-Ying Shen ◽  
...  

2016 ◽  
Vol 14 (1) ◽  
Author(s):  
Jing Zhong ◽  
Chang Liu ◽  
Ya-jun Chen ◽  
Qing-hai Zhang ◽  
Jing Yang ◽  
...  

RSC Advances ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 4163-4163
Author(s):  
Laura Fisher

Retraction of ‘Overexpression of PCDH8 inhibits proliferation and invasion, and induces apoptosis in papillary thyroid cancer cells’ by Liang Chang et al., RSC Adv., 2018, 8, 18030–18037, DOI: 10.1039/C8RA02291G.


Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 860
Author(s):  
Chia-Herng Yue ◽  
Muhammet Oner ◽  
Chih-Yuan Chiu ◽  
Mei-Chih Chen ◽  
Chieh-Lin Teng ◽  
...  

Medullary thyroid cancer (MTC) is a neuroendocrine tumor that arises from the parafollicular C-cells, which produces the hormone calcitonin. RET is a transmembrane receptor protein-tyrosine kinase, which is highly expressed in MTC. Our previous studies reported that cyclin-dependent kinase 5 (CDK5) plays a crucial role in cancer progression, including MTC. However, the role of CDK5 in GDNF-induced RET signaling in medullary thyroid cancer proliferation remains unknown. Here, we investigated RET activation and its biochemically interaction with CDK5 in GDNF-induced medullary thyroid cancer proliferation. Our results demonstrated that GDNF stimulated RET phosphorylation and thus subsequently resulted in CDK5 activation by its phosphorylation. Activated CDK5 further caused STAT3 activation by its specific phosphorylation at Ser727. Moreover, we also found that GDNF treatment enhanced ERK1/2 and EGR1 activity, which is involved in p35 activation. Interestingly, we identified for the first time that CDK5 physically interacted with RET protein in MTC. Overall, our results provide a new mechanism for medullary thyroid cancer cell proliferation, suggesting that targeting CDK5 may be a promising therapeutic candidate for human medullary thyroid cancer in the near future.


2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Yunheng Zhu ◽  
Xiaohua Zhang ◽  
Lifeng Wang ◽  
Xiuxiang Zhu ◽  
Ziyin Xia ◽  
...  

2019 ◽  
Vol 37 (2) ◽  
pp. 150-157 ◽  
Author(s):  
Hua Jiang ◽  
Qiang Bu ◽  
Minghui Zeng ◽  
Dongdong Xia ◽  
Aibin Wu

2018 ◽  
Vol 120 (4) ◽  
pp. 5704-5712 ◽  
Author(s):  
Xin Wang ◽  
Mudan Ren ◽  
Yarui Li ◽  
Junbi Hu ◽  
Guifang Lu ◽  
...  

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Meiyuan Yang ◽  
Xiaoli Tang ◽  
Zheng Wang ◽  
Xiaoqing Wu ◽  
Dong Tang ◽  
...  

Abstract Colorectal cancer (CRC) is the third most common malignant tumor worldwide and is a serious threat to human health. MicroRNAs (miRNAs) play a key role in oncogenesis and cancer progression. MiRNA-125 (miR-125) is an important miRNA that is dysregulated in several kinds of cancers. Thus, we investigated the expression and effects of miR-125 and Transcriptional co-activator with PDZ-binding motif (TAZ) for a better understanding of the underlying mechanism of tumor progression in CRC, which may provide an emerging biomarker for diagnosis and treatment of CRC. We measured the expression levels of miR-125 in CRC tissues, adjacent tissues, and cell lines (e.g. HCT116, SW480, FHC) by quantitative real-time polymerase chain reaction (qRT-PCR). The effect of miR-125 on proliferation and invasion in CRC cells was detected by Cell Counting Kit-8 (CCK-8), clone formation assay, and transwell assay. Western blotting and qRT-PCR were used to investigate the expression of TAZ after knocking down miR-125 in HCT116 cells or overexpressing miR-125 in SW480 cells. MiR-125 was significantly down-regulated in CRC compared with pericarcinomatous tissue from 18 patients. An miR-125 inhibitor promoted CRC cell proliferation and invasion, while miR-125 mimic had the opposite effect. Moreover, we found that TAZ was an miR-125 target and the siRNA knockdown of TAZ could reverse the effect of the miR-125 inhibitor on proliferation and invasion in HCT116 cells. The present study shows that miR-125 suppresses CRC proliferation and invasion by targeting TAZ.


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