Photosensitizing effect of Photolon using optical fiber probe to laser-irradiate thyroid cancer cells: oxidative stress-directed cell death

2020 ◽  
Author(s):  
Ga-ye Park ◽  
Yun-Hee Rhee ◽  
HyeYeon Lee ◽  
Junho Lee ◽  
Hyunjoo Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Thyroid Cancer ◽  
Optical Fiber ◽  
Cancer Cells ◽  
Fiber Probe ◽  
Optical Fiber Probe ◽  
Thyroid Cancer Cells

scholarly journals Interplay between thyroid cancer cells and macrophages: effects on IL-32 mediated cell death and thyroid cancer cell migration

2019 ◽  
Vol 42 (5) ◽  
pp. 691-703 ◽  
Author(s):  
Yvette J. E. Sloot ◽  
Katrin Rabold ◽  
Thomas Ulas ◽  
Dennis M. De Graaf ◽  
Bas Heinhuis ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Migration ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Cell Migration ◽  
Thyroid Cancer Cell ◽  
Thyroid Cancer Cells

Delayed luminescence to monitor programmed cell death induced by berberine on thyroid cancer cells

2014 ◽  
Vol 19 (11) ◽  
pp. 117005 ◽  
Author(s):  
Agata Scordino ◽  
Agata Campisi ◽  
Rosaria Grasso ◽  
Roberta Bonfanti ◽  
Marisa Gulino ◽  
...  
Keyword(s):  
Cell Death ◽  
Thyroid Cancer ◽  
Programmed Cell Death ◽  
Cancer Cells ◽  
Delayed Luminescence ◽  
Thyroid Cancer Cells

Curcumin induces autophagic cell death in human thyroid cancer cells

2021 ◽  
pp. 105254
Author(s):  
Li Zhang ◽  
Shichen Xu ◽  
Xian Cheng ◽  
Jing Wu ◽  
Liying Wu ◽  
...  
Keyword(s):  
Cell Death ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Autophagic Cell Death ◽  
Human Thyroid ◽  
Thyroid Cancer Cells

scholarly journals Epigenetic Modifications in Thyroid Cancer Cells Restore NIS and Radio-Iodine Uptake and Promote Cell Death

2018 ◽  
Vol 7 (4) ◽  
pp. 61 ◽  
Author(s):  
Sabine Wächter ◽  
Alexander Damanakis ◽  
Moritz Elxnat ◽  
Silvia Roth ◽  
Annette Wunderlich ◽  
...  
Keyword(s):  
Cell Death ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Epigenetic Modifications ◽  
Iodine Uptake ◽  
Thyroid Cancer Cells ◽  
Promote Cell Death

scholarly journals Quercetin-Induced Cell Death in Human Papillary Thyroid Cancer (B-CPAP) Cells

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Ergül Mutlu Altundağ ◽  
Tolga Kasacı ◽  
Ayşe Mine Yılmaz ◽  
Betül Karademir ◽  
Semra Koçtürk ◽  
...  
Keyword(s):  
Cell Death ◽  
Thyroid Cancer ◽  
Protein Expression ◽  
Cancer Cells ◽  
Papillary Thyroid Cancer ◽  
Annexin V ◽  
Proteasome Activity ◽  
Papillary Thyroid ◽  
Candidate Drug ◽  
Thyroid Cancer Cells

In this study, we have investigated the antiproliferative effect of quercetin on human papillary thyroid cancer cells and determined the apoptotic mechanisms underlying its actions. We have used different concentrations of quercetin to induce apoptosis and measured cell viability. Apoptosis and cell cycle analysis was determined by flow cytometry using Annexin V and propidium iodide. Finally, we have measured changes in caspase-3 and cleaved poly(ADP-ribose) polymerase (PARP) protein expression levels as hallmarks of apoptosis and Hsp90 protein expression level as a marker of proteasome activity in treated and control cells. Quercetin treatment of human papillary thyroid cancer cells resulted in decreased cell proliferation and increased rate of apoptosis by caspase activation. Furthermore, it was demonstrated that quercetin induces cancer cell apoptosis by downregulating the levels of Hsp90. In conclusion, we have shown that quercetin induces downregulation of Hsp90 expression that may be involved in the decrease of chymotrypsin-like proteasome activity which, in order, induces inhibition of growth and causes cell death in thyroid cancer cells. Thus, quercetin appears to be a promising candidate drug for Hsp90 downregulation and apoptosis of thyroid cancer cells.

scholarly journals Involvement of Glyceraldehyde-3-Phosphate Dehydrogenase in Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand-Mediated Death of Thyroid Cancer Cells

Endocrinology ◽  
2007 ◽  
Vol 148 (9) ◽  
pp. 4352-4361 ◽  
Author(s):  
Zhen-Xian Du ◽  
Hua-Qin Wang ◽  
Hai-Yan Zhang ◽  
Da-Xin Gao
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Thyroid Cancer ◽  
Nitric Oxide Synthase ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Nuclear Translocation ◽  
Thyroid Cancer Cell ◽  
Oxide Synthase ◽  
Thyroid Cancer Cells

TNF-related apoptosis-inducing ligand (TRAIL) is cytotoxic to most thyroid cancer cell lines, including those originating from anaplastic carcinomas, implying TRAIL as a promising therapeutic agent against thyroid cancers. However, signal transduction in TRAIL-mediated apoptosis is not clearly understood. In addition to its well-known glycolytic functions, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a multifunctional protein, including its surprising role as a mediator for cell death. In this study we explored the involvement of GAPDH in TRAIL-mediated thyroid cancer cell death. In follicular undifferentiated thyroid cells, S-nitrosylation and nuclear translocation of GAPDH appear to mediate TRAIL-induced cell death at least partially, as evidenced by pretreatment with N-nitro-L-arginine methyl ester, a competitive nitric oxide synthase inhibitor that partially but significantly attenuated TRAIL-induced apoptosis through the reduction of S-nitrosylation and nuclear translocation of GAPDH. In addition, GAPDH small interfering RNA partially prevented the apoptotic effect of TRAIL, although TRAIL-induced nitric oxide synthase stimulation and production of nitric oxide were not attenuated. Furthermore, nuclear localization of GAPDH was observed in another thyroid cancer cell line, KTC2, which is also sensitive to TRAIL, but not in those TRAIL insensitive cell lines: ARO, KTC1, and KTC3. These data indicate that nitric oxide-mediated S-nitrosylation of GAPDH and subsequent nuclear translocation of GAPDH might function as a mediator of TRAIL-induced cell death in thyroid cancer cells.

scholarly journals Suppression of MG132-mediated cell death by peroxiredoxin 1 through influence on ASK1 activation in human thyroid cancer cells

2010 ◽  
Vol 17 (3) ◽  
pp. 553-560 ◽  
Author(s):  
Zhen-Xian Du ◽  
Ying Yan ◽  
Hai-Yan Zhang ◽  
Bao-Qin Liu ◽  
Yan-Yan Gao ◽  
...  
Keyword(s):  
Cell Death ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
Proteasome Inhibitor ◽  
Antitumor Agents ◽  
Proteasome Inhibitors ◽  
Hematologic Malignancies ◽  
Mitogen Activated Protein Kinase ◽  
Human Thyroid ◽  
Thyroid Cancer Cells

Proteasome inhibitors represent a novel class of antitumor agents with pre-clinical and clinical evidence of activity against hematologic malignancies and solid tumors. However, emerging evidence indicates that antiapoptotic factors may also accumulate as a consequence of exposure to these drugs, thus it seems plausible that the activation of survival signaling cascades might compromise their antitumoral effects. Peroxiredoxins (PRDXs) are a family of thiol-containing peroxidases identified primarily by their ability to remove cellular hydroperoxides. The function of PRDX1 in particular has been implicated in regulating cell proliferation, differentiation, and apoptosis. Another important finding is that aberrant upregulation of PRDX1 has been discovered in various cancers. Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase (MAPK) kinase kinase that is regulated under conditions of cellular stress. ASK1 phosphorylates c-Jun N-terminal kinase and p38 MAPK, and elicits an apoptotic response. ASK1 activity is regulated at multiple levels, one of which is through interaction with PRDX1. In this study, for the first time we report that upregulation of PRDX1 expression was found in thyroid cancer cells treated with proteasome inhibitors, and PRDX1 knockdown resulted in accelerated proteasome inhibitor-induced cell death. In addition, we demonstrated that ASK1 activity was implicated in the PRDX1-dependent response of thyroid cancer cells to proteasome inhibitor-mediated cell death.

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