scholarly journals Imatinib Enhances Docetaxel-Induced Apoptosis Through Inhibition of Nuclear Factor-κB Activation in Anaplastic Thyroid Carcinoma Cells

Thyroid ◽  
2012 ◽  
Vol 22 (7) ◽  
pp. 717-724 ◽  
Author(s):  
EunSook Kim ◽  
Michiko Matsuse ◽  
Vladimir Saenko ◽  
Keiji Suzuki ◽  
Akira Ohtsuru ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Nuclear Factor Κb ◽  
Anaplastic Thyroid Carcinoma ◽  
Carcinoma Cells ◽  
Nuclear Factor ◽  
Induced Apoptosis

scholarly journals Imatinib enhances docetaxel-induced apoptosis through inhibition of nuclear factor-κB activation in anaplastic thyroid carcinoma cells

Thyroid ◽  
2012 ◽  
pp. 120406132503004
Author(s):  
EunSook Kim ◽  
Michiko Matsuse ◽  
Vladimir Saenko ◽  
Keiji Suzuki ◽  
Akira Ohtsuru ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Nuclear Factor Κb ◽  
Anaplastic Thyroid Carcinoma ◽  
Carcinoma Cells ◽  
Nuclear Factor ◽  
Induced Apoptosis

scholarly journals Roles of reactive oxygen species, mitochondrial membrane potential, and p53 in evodiamine-induced apoptosis and G2/M arrest of human anaplastic thyroid carcinoma cells

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Chih-Chiang Chien ◽  
Ming-Shun Wu ◽  
Shih-Wei Chou ◽  
Ganbolor Jargalsaikhan ◽  
Yen-Chou Chen
Keyword(s):  
Reactive Oxygen Species ◽  
Flow Cytometry ◽  
Thyroid Carcinoma ◽  
Mitochondrial Membrane ◽  
Anaplastic Thyroid Carcinoma ◽  
Carcinoma Cells ◽  
Ros Production ◽  
Oxygen Species ◽  
P53 Status ◽  
Induced Apoptosis

Abstract Background Our previous studies have shown that evodiamine (EVO) as paclitaxel and nocodazole could trigger apoptosis in various human cancer cells including human renal cell carcinoma cells, colorectal carcinoma cells, and glioblastoma cells. This study aims to investigate the anti-cancer effects of EVO on human anaplastic thyroid carcinoma (ATC) cells, and underlining mechanism. Methods Two different endogenous p53 status human anaplastic thyroid carcinoma (ATC) cells including SW1736 (wtp53) and KAT4B (mutp53) were applied in the present study. The cytotoxicity of EVO on ATC cells was measured by MTT assay, and apoptosis and G2/M arrest were detected by propidium iodide (PI) staining followed by flow cytometry. Expression of indicated proteins was evaluated by Western blotting analysis, and pharmacological studies using chemical inhibitors and siRNA were performed for elucidating underlying mechanism. The roles of mitochondrial membrane potential and reactive oxygen species were investigated by flow cytometry using DiOC6 and DCFH-DA dye, respectively. Results SW1736 (wtp53) cells showed a higher apoptotic percentage than KAT4B (mutp53) cells in response to EVO stimulation via a flow cytometric analysis. Mechanistic studies showed that increased p53 and its downstream proteins, and disrupted MMP with increased intracellular peroxide production participated in EVO-induced apoptosis and G2/M arrest of SW1736 cells. In EVO-treated KAT4B cells, significant increases in G2/M percentage but little apoptotic events by EVO was observed. Structure-activity analysis showed that an alkyl group at position 14 was critical for induction of apoptosis related to ROS production and MMP disruption in SW1736 cells. Conclusion Evidence indicated that the endogenous p53 status affected the sensitivity of ATC cells to EVO-induced apoptosis and G2/M arrest, revealing the potential role of p53 related to increased ROS production and disrupted MMP in the anticancer actions of EVO, and alkylation at position 14 of EVO is a critical substitution for apoptosis of ATC cells.

scholarly journals Requirement of Nuclear Factor κB for Smac Mimetic–Mediated Sensitization of Pancreatic Carcinoma Cells for Gemcitabine-Induced Apoptosis

Neoplasia ◽  
2011 ◽  
Vol 13 (12) ◽  
pp. 1162-IN21 ◽  
Author(s):  
Dominic Stadel ◽  
Silvia Cristofanon ◽  
Behnaz Ahangarian Abhari ◽  
Kurt Deshayes ◽  
Kerry Zobel ◽  
...  
Keyword(s):  
Pancreatic Carcinoma ◽  
Nuclear Factor Κb ◽  
Carcinoma Cells ◽  
Nuclear Factor ◽  
Smac Mimetic ◽  
Induced Apoptosis

scholarly journals Curcumin Enhances Docetaxel-Induced Apoptosis of 8505C Anaplastic Thyroid Carcinoma Cells

2014 ◽  
Vol 29 (1) ◽  
pp. 54 ◽  
Author(s):  
Jung Min Hong ◽  
Chan Sung Park ◽  
Il Seong Nam-Goong ◽  
Yon Seon Kim ◽  
Jong Cheol Lee ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Anaplastic Thyroid Carcinoma ◽  
Carcinoma Cells ◽  
Induced Apoptosis

scholarly journals Effects of nuclear factor‑κB on the uptake of 131iodine and apoptosis of thyroid carcinoma cells

2018 ◽  
Author(s):  
Fukun Chen ◽  
Shuting Yin ◽  
Jialun Zhu ◽  
Li Jia ◽  
Huaping Zhang ◽  
...  
Keyword(s):  
Thyroid Carcinoma ◽  
Nuclear Factor Κb ◽  
Carcinoma Cells ◽  
Nuclear Factor

Evaluation of E-Cadherin and β-Catenin Immunoreactivity for Determining Undifferentiated Cells in Anaplastic Thyroid Carcinoma

Pathobiology ◽  
2021 ◽  
pp. 1-8
Author(s):  
Risa Kanematsu ◽  
Mitsuyoshi Hirokawa ◽  
Aki Tanaka ◽  
Ayana Suzuki ◽  
Miyoko Higuchi ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Thyroid Carcinoma ◽  
Undifferentiated Carcinoma ◽  
Anaplastic Thyroid Carcinoma ◽  
Carcinoma Cells ◽  
Membrane Expression ◽  
Thyroid Carcinomas ◽  
Nuclear Expression ◽  
Thyroid Transcription Factor 1 ◽  
E Cadherin

<b><i>Introduction:</i></b> An immunohistochemical study has occasionally been performed to diagnose anaplastic thyroid carcinoma (ATC). However, antibodies to confirm the undifferentiated nature of ATC have not yet been evaluated. The aim of this study was to evaluate E-cadherin and β-catenin expressions in immunoreactivity to determine undifferentiated carcinoma cells in the diagnosis of ATC. <b><i>Methods:</i></b> We immunohistochemically examined 29 ATCs, 30 poorly differentiated thyroid carcinomas (PDTCs), 22 well-differentiated thyroid carcinomas (WDTCs), and 3 squamous cell carcinomas. Antibodies for thyroid transcription factor-1 (TTF-1), paired-box gene 8 (PAX8), β-catenin, and E-cadherin were used. <b><i>Results:</i></b> All WDTCs tested positive for TTF-1, PAX8, and E-cadherin. The positive rates of TTF-1, PAX8, and E-cadherin were 93.3, 93.3, and 100%, respectively, in PDTCs and 17.2, 51.7, and 10.3%, respectively, in ATCs. WDTC expressed the lateral cell membrane staining for β-catenin and E-cadherin, whereas PDTC showed circumferential cell membranous expression (fishnet pattern). β-catenin cell membrane expression in ATCs is lost or discontinuous. Carcinoma cells with β-catenin nuclear expression without cell membranous expression were scattered in 72.4% of ATCs but were not observed in the other carcinomas. <b><i>Conclusion:</i></b> We propose 3 immunohistochemical findings to determine undifferentiated carcinoma cells in the diagnosis of ATC: (1) β-catenin nuclear expression with no or reduced cell membranous expression, (2) the loss or discontinuous pattern of E-cadherin expression, and (3) the loss of PAX8 nuclear expression.

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