Abstract 2948: c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK) are involved in local anesthetics-induced apoptosis in human thyroid cancer cells.

2013 ◽  
Author(s):  
Shih-Ping Cheng ◽  
Yuan-Ching Chang ◽  
Yi-Chiung Hsu ◽  
Shih-Yuan Huang ◽  
Meng-Chun Hu ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
P38 Mapk ◽  
Local Anesthetics ◽  
Mitogen Activated Protein Kinase ◽  
Human Thyroid ◽  
Mitogen Activated Protein ◽  
Induced Apoptosis ◽  
Thyroid Cancer Cells

scholarly journals Local Anesthetics Induce Apoptosis in Human Thyroid Cancer Cells through the Mitogen-Activated Protein Kinase Pathway

PLoS ONE ◽  
2014 ◽  
Vol 9 (2) ◽  
pp. e89563 ◽  
Author(s):  
Yuan-Ching Chang ◽  
Yi-Chiung Hsu ◽  
Chien-Liang Liu ◽  
Shih-Yuan Huang ◽  
Meng-Chun Hu ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Local Anesthetics ◽  
Mitogen Activated Protein Kinase ◽  
Human Thyroid ◽  
Mitogen Activated Protein ◽  
Thyroid Cancer Cells ◽  
Kinase Pathway

Activation of Protein Kinase CδInduces Growth Arrest in NPA Thyroid Cancer Cells Through Extracellular Signal-Regulated Kinase Mitogen-Activated Protein Kinase

Thyroid ◽  
2006 ◽  
Vol 16 (4) ◽  
pp. 333-341 ◽  
Author(s):  
Kenta Koike ◽  
Teruhiko Fujii ◽  
Anna M. Nakamura ◽  
Goro Yokoyama ◽  
Hideaki Yamana ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Growth Arrest ◽  
Mitogen Activated Protein Kinase ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Mitogen Activated Protein ◽  
Thyroid Cancer Cells

scholarly journals Distinct Genetic Alterations in the Mitogen-Activated Protein Kinase Pathway Dictate Sensitivity of Thyroid Cancer Cells to Mitogen-Activated Protein Kinase Kinase 1/2 Inhibition

Thyroid ◽  
2009 ◽  
Vol 19 (8) ◽  
pp. 825-835 ◽  
Author(s):  
Rebecca E. Schweppe ◽  
Anna A. Kerege ◽  
Vibha Sharma ◽  
Joanna M. Poczobutt ◽  
Arthur Gutierrez-Hartmann ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Genetic Alterations ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Thyroid Cancer Cells ◽  
Kinase Pathway ◽  
Protein Kinase Kinase

scholarly journals Zamzam water protects cancer cells from chemotherapy-induced apoptosis via mitogen-activated protein kinase-dependent pathway

2019 ◽  
Vol 118 ◽  
pp. 109376
Author(s):  
Abdul Khalid Siraj ◽  
Rafia Begum ◽  
Roxanne Melosantos ◽  
Wafaa Albalawy ◽  
Jehan Abboud ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cancer Cells ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Induced Apoptosis ◽  
Dependent Pathway

scholarly journals Protein Kinase A-Independent Inhibition of Proliferation and Induction of Apoptosis in Human Thyroid Cancer Cells by 8-Cl-Adenosine

2008 ◽  
Vol 93 (3) ◽  
pp. 1020-1029 ◽  
Author(s):  
Audrey J. Robinson-White ◽  
Hui-Pin Hsiao ◽  
Wolfgang W. Leitner ◽  
Elizabeth Greene ◽  
Andrew Bauer ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Protein Kinase ◽  
Protein Kinase A ◽  
Cancer Cells ◽  
Human Thyroid ◽  
Inhibition Of Proliferation ◽  
Thyroid Cancer Cells ◽  
Kinase A

Abstract Purpose: Protein kinase A (PKA) affects cell proliferation in many cell types and is a potential target for cancer treatment. PKA activity is stimulated by cAMP and cAMP analogs. One such substance, 8-Cl-cAMP, and its metabolite 8-Cl-adenosine (8-Cl-ADO) are known inhibitors of cancer cell proliferation; however, their mechanism of action is controversial. We have investigated the antiproliferative effects of 8-Cl-cAMP and 8-CL-ADO on human thyroid cancer cells and determined PKA’s involvement. Experimental Design: We employed proliferation and apoptosis assays and PKA activity and cell cycle analysis to understand the effect of 8-Cl-ADO and 8-Cl-cAMP on human thyroid cancer and HeLa cell lines. Results: 8-Cl-ADO inhibited proliferation of all cells, an effect that lasted for at least 4 d. Proliferation was also inhibited by 8-Cl-cAMP, but this inhibition was reduced by 3-isobutyl-1-methylxanthine; both drugs stimulated apoptosis, and 3-isobutyl-1-methylxanthine drastically reduced 8-Cl-cAMP-induced cell death. 8-Cl-ADO induced cell accumulation in G1/S or G2/M cell cycle phases and differentially altered PKA activity and subunit levels. PKA stimulation or inhibition and adenosine receptor agonists or antagonists did not significantly affect proliferation. Conclusions: 8-Cl-ADO and 8-Cl-cAMP inhibit proliferation, induce cell cycle phase accumulation, and stimulate apoptosis in thyroid cancer cells. The effect of 8-Cl-cAMP is likely due to its metabolite 8-Cl-ADO, and PKA does not appear to have direct involvement in the inhibition of proliferation by 8-Cl-ADO. 8-Cl-ADO may be a useful therapeutic agent to be explored in aggressive thyroid cancer.

scholarly journals Iodine Promotes Tumorigenesis of Thyroid Cancer by Suppressing Mir-422a and Up-Regulating MAPK1

2017 ◽  
Vol 43 (4) ◽  
pp. 1325-1336 ◽  
Author(s):  
Junyi  Wang ◽  
Haiou Yang ◽  
Yiran Si ◽  
Dongzhi Hu ◽  
Yang Yu ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Thyroid Carcinoma ◽  
Cancer Cells ◽  
Mitogen Activated Protein Kinase ◽  
In Vivo Studies ◽  
Mitogen Activated Protein ◽  
And Migration ◽  
Cell Migration And Proliferation ◽  
Thyroid Cancer Cells

Background/Aims: Iodine may trigger tumorigenesis and development of thyroid carcinoma, but the mechanisms involved remained elusive. MicroRNA (MiRNAs) are known to be involved in each stage of cancer development; however, the role of miRNAs in iodine-induced tumorigenesis of thyroid carcinoma remained unknown. In this study, we aimed at investigating miRNA related signaling pathway in thyroid cancer cells. Methods: Levels of miRNAs and mRNAs were determined using RT-qPCR and proteins were quantified by western blotting. Cell migration and proliferation were checked using Transwell assay and CCK8 assay respectively. Tumor xenografts in nude mice were established by subcutaneous injection of cancer cells. Results: Mitogen activated protein kinase 1 (MAPK1) was significantly up-regulated, while miR-422a was down-regulated in thyroid cancer cells cultured with high iodine; miR-422a directly bound to the 3’UTR of MAPK1 mRNA. Moreover, miR-422a negatively regulated MAPK1 expression, and down-regulated miR-422a promoted proliferation and migration of TPC-1 cells. In vivo studies also confirmed that iodine promoted tumor growth by suppressing miR-422a and up-regulating MAPK1. Conclusions: Our study illustrates a new pathway comprising iodine, miRNA and MAPK1, and defines a novel mechanism in thyroid cancer.

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