Ceramide-Induced Apoptosis of Human Thyroid Cancer Cells Resistant to Apoptosis by Irradiation

Thyroid ◽  
2000 ◽  
Vol 10 (9) ◽  
pp. 733-740 ◽  
Author(s):  
Yuriy Sautin ◽  
Noboru Takamura ◽  
Stanislav Shklyaev ◽  
Yuji Nagayama ◽  
Akira Ohtsuru ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Human Thyroid ◽  
Induced Apoptosis ◽  
Thyroid Cancer Cells

scholarly journals Implication of Oxygen-Regulated Protein 150 (ORP150) in Apoptosis Induced by Proteasome Inhibitors in Human Thyroid Cancer Cells

2010 ◽  
Vol 31 (5) ◽  
pp. 779-780
Author(s):  
Yan-Yan Gao ◽  
Bao-Qin Liu ◽  
Zhen-Xian Du ◽  
Hai-Yan Zhang ◽  
Xiao-Fang Niu ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Transcription Factor ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Proteasome Inhibitors ◽  
Proteasome Inhibition ◽  
26S Proteasome ◽  
Human Thyroid ◽  
Induced Apoptosis ◽  
Thyroid Cancer Cells

ABSTRACT Context The inhibition of the 26S proteasome may lead to endoplasmic reticulum stress, which has been shown to be implicated in the antitumoral effects of proteasome inhibitors. Oxygen-regulated protein 150 (ORP150) is an inducible endoplasmic reticulum chaperone that is up-regulated after numerous cellular insults and has a cytoprotective role for the maintenance of cellular viability. Objective The purpose of this study was to determine the involvement of ORP150 in cytotoxicity of thyroid cancer cells mediated by proteasome inhibition. Design The effects of proteasome inhibition on the expression of ORP150 were analyzed using real-time RT-PCR and Western blot. To ascertain the effect of ORP150, cells were transfected with ORP150 plasmid or small interfering RNA (siRNA) against ORP150, apoptotic cells, and induction of CCAAT/enhancer-binding protein homologous transcription factor (CHOP) mediated by proteasome inhibition were investigated. Results ORP150 was induced in thyroid cancer cells after proteasome inhibition. Suppression of activating transcription factor 4 expression by siRNA inhibited the up-regulation of ORP150 mediated by proteasome inhibitors. siRNA for ORP150 stimulated MG132-mediated apoptosis and induction of CHOP, a transcription factor with apoptosis-inducing activity. In contrast, ORP150-overexpressing cells demonstrated less susceptibility to MG132-induced apoptosis and displayed less up-regulation of CHOP. In addition, the sensitizing effect of small interfering ORP150 on apoptosis was suppressed by siRNA for CHOP. Conclusions These results suggest that up-regulation of ORP150 in thyroid cancer cells inhibits MG132-induced apoptosis via suppression of CHOP induction, thereby decreasing the potential antitumor activity of MG132.

scholarly journals CRSP8 promotes thyroid cancer progression by antagonizing IKKα-induced cell differentiation

2020 ◽  
Author(s):  
Yina Liao ◽  
Yijun Hua ◽  
Yizhuo Li ◽  
Changlin Zhang ◽  
Wendan Yu ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Direct Interaction ◽  
Anaplastic Thyroid Cancer ◽  
Human Thyroid ◽  
Induced Apoptosis ◽  
Thyroid Cancer Cells

Abstract CRSP8 plays an important role in recruiting mediators to genes through direct interaction with various DNA-bound transactivators. In this study, we uncovered the unique function of CRSP8 in suppressing thyroid cancer differentiation and promoting thyroid cancer progression via targeting IKKα signaling. CRSP8 was highly expressed in human thyroid cancer cells and tissues, especially in anaplastic thyroid cancer (ATC). Knockdown of CRSP8 suppressed cell growth, migration, invasion, stemness, and induced apoptosis and differentiation in ATC cells, while its overexpression displayed opposite effects in differentiated thyroid cancer (DTC) cells. Mechanistically, CRSP8 downregulated IKKα expression by binding to the IKKα promoter region (−257 to −143) to negatively regulate its transcription. Knockdown or overexpression of IKKα significantly reversed the expression changes of the differentiation and EMT-related markers and cell growth changes mediated by CRSP8 knockdown or overexpression in ATC or DTC cells. The in vivo study also validated that CRSP8 knockdown inhibited the growth of thyroid cancer by upregulating IKKα signaling in a mouse model of human ATC. Furthermore, we found that CRSP8 regulated the sensitivity of thyroid cancer cells to chemotherapeutics, including cisplatin and epirubicin. Collectively, our results demonstrated that CRSP8 functioned as a modulator of IKKα signaling and a suppressor of thyroid cancer differentiation, suggesting a potential therapeutic strategy for ATC by targeting CRSP8/IKKα pathway.

Anti-proliferative effects of evodiamine on human thyroid cancer cells

2014 ◽  
Author(s):  
Ying-Ray Lee ◽  
Chieh-Hsiang Lu ◽  
Yi-Sheng Chang ◽  
Yi-Wen Liu
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Human Thyroid ◽  
Thyroid Cancer Cells

scholarly journals Changes in Exosome Release in Thyroid Cancer Cells after Prolonged Exposure to Real Microgravity in Space

2021 ◽  
Vol 22 (4) ◽  
pp. 2132
Author(s):  
Petra M. Wise ◽  
Paolo Neviani ◽  
Stefan Riwaldt ◽  
Thomas Juhl Corydon ◽  
Markus Wehland ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Protein Expression ◽  
Cancer Cells ◽  
Prolonged Exposure ◽  
Space Station ◽  
Surface Protein ◽  
Surface Expression ◽  
Human Thyroid ◽  
Gene And Protein Expression ◽  
Thyroid Cancer Cells

Space travel has always been the man’s ultimate destination. With the ability of spaceflight though, came the realization that exposure to microgravity has lasting effects on the human body. To counteract these, many studies were and are undertaken, on multiple levels. Changes in cell growth, gene, and protein expression have been described in different models on Earth and in space. Extracellular vesicles, and in particular exosomes, are important cell-cell communicators, being secreted from almost all the cells and therefore, are a perfect target to further investigate the underlying reasons of the organism’s adaptations to microgravity. Here, we studied supernatants harvested from the CellBox-1 experiment, which featured human thyroid cancer cells flown to the International Space Station during the SpaceX CRS-3 cargo mission. The initial results show differences in the number of secreted exosomes, as well as in the distribution of subpopulations in regards to their surface protein expression. Notably, alteration of their population regarding the tetraspanin surface expression was observed. This is a promising step into a new area of microgravity research and will potentially lead to the discovery of new biomarkers and pathways of cellular cross-talk.

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 Bcl-2-Associated X Protein Is the Main Mediator of Manumycin A-Induced Apoptosis in Anaplastic Thyroid Cancer Cells

2005 ◽  
Vol 90 (6) ◽  
pp. 3583-3591 ◽  
Author(s):  
Jingxuan Pan ◽  
Huizhi Huang ◽  
Lily Sun ◽  
Bingliang Fang ◽  
Sai-Ching Jim Yeung
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Anaplastic Thyroid Cancer ◽  
X Protein ◽  
Induced Apoptosis ◽  
Thyroid Cancer Cells

Impairment of ATP-induced Ca2+-signalling in human thyroid cancer cells

1997 ◽  
Vol 133 (1) ◽  
pp. 33-39 ◽  
Author(s):  
C Schöfl ◽  
L Rössig ◽  
T Mader ◽  
J Börger ◽  
E Pötter ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Human Thyroid ◽  
Thyroid Cancer Cells

Abstract 2017: Demethylation of HIC1 gene sensitizes thyroid cancer cells to TRAIL-induced apoptosis

2011 ◽  
Author(s):  
Abdul K. Siraj ◽  
Maha Al-Rasheed ◽  
Azhar Husain ◽  
Prashant Bavi ◽  
Abdul Rahman Al Nuaim ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Cells ◽  
Induced Apoptosis ◽  
Thyroid Cancer Cells
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