scholarly journals Cl-IB-MECA inhibits human thyroid cancer cell proliferation independently of A3 adenosine receptor activation

2008 ◽  
Vol 7 (2) ◽  
pp. 278-284 ◽  
Author(s):  
Silvana Morello ◽  
Antonello Petrella ◽  
Michela Festa ◽  
Ada Popolo ◽  
Mario Monaco ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Cancer Cell ◽  
Adenosine Receptor ◽  
Receptor Activation ◽  
Human Thyroid ◽  
Cancer Cell Proliferation ◽  
Thyroid Cancer Cell ◽  
A3 Adenosine Receptor ◽  
Adenosine Receptor Activation

scholarly journals Long glucocorticoid-induced leucine zipper regulates human thyroid cancer cell proliferation

2018 ◽  
Vol 9 (3) ◽  
Author(s):  
Emira Ayroldi ◽  
Maria Grazia Petrillo ◽  
Maria Cristina Marchetti ◽  
Lorenza Cannarile ◽  
Simona Ronchetti ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Cancer Cell ◽  
Leucine Zipper ◽  
Human Thyroid ◽  
Cancer Cell Proliferation ◽  
Thyroid Cancer Cell

scholarly journals RET Regulates Human Medullary Thyroid Cancer Cell Proliferation through CDK5 and STAT3 Activation

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 860
Author(s):  
Chia-Herng Yue ◽  
Muhammet Oner ◽  
Chih-Yuan Chiu ◽  
Mei-Chih Chen ◽  
Chieh-Lin Teng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Medullary Thyroid Cancer ◽  
Receptor Protein ◽  
Cancer Cell Proliferation ◽  
Thyroid Cancer Cell ◽  
Cancer Proliferation ◽  
Medullary Thyroid

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.

Cyclopamine Inhibits Cancer Cell Proliferation in Thyroid Cancer Cell Lines

2007 ◽  
Vol 7 (2) ◽  
pp. 69
Author(s):  
Sung Su Park ◽  
Jin-Woo Park ◽  
Jae-Woon Choi ◽  
Lee-Chan Jang ◽  
Sung-Il Woo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Cancer Cell Proliferation ◽  
Thyroid Cancer Cell ◽  
Thyroid Cancer Cell Lines
Sign in / Sign up

Export Citation Format

Share Document