scholarly journals Programmed cell death 4 (PDCD4) as a novel prognostic marker for papillary thyroid carcinoma

2019 ◽  
Vol Volume 11 ◽  
pp. 7845-7855 ◽  
Author(s):  
Francesca Galuppini ◽  
Matteo Fassan ◽  
Loris Bertazza ◽  
Susi Barollo ◽  
Luciano Cascione ◽  
...  
Keyword(s):  
Cell Death ◽  
Papillary Thyroid Carcinoma ◽  
Programmed Cell Death ◽  
Thyroid Carcinoma ◽  
Prognostic Marker ◽  
Papillary Thyroid ◽  
Programmed Cell Death 4

scholarly journals miR-183 regulates biological behavior in papillary thyroid carcinoma by targeting the programmed cell death 4

2015 ◽  
Vol 34 (1) ◽  
pp. 211-220 ◽  
Author(s):  
CHUANKUI WEI ◽  
HONGMING SONG ◽  
XIAOGUO SUN ◽  
DENGFENG LI ◽  
JIALU SONG ◽  
...  
Keyword(s):  
Cell Death ◽  
Papillary Thyroid Carcinoma ◽  
Programmed Cell Death ◽  
Thyroid Carcinoma ◽  
Biological Behavior ◽  
Papillary Thyroid ◽  
Programmed Cell Death 4

scholarly journals Dipeptidyl Peptidase IV as a Prognostic Marker and Therapeutic Target in Papillary Thyroid Carcinoma

2017 ◽  
Vol 102 (8) ◽  
pp. 2930-2940 ◽  
Author(s):  
Jie-Jen Lee ◽  
Tao-Yeuan Wang ◽  
Chien-Liang Liu ◽  
Ming-Nan Chien ◽  
Ming-Jen Chen ◽  
...  
Keyword(s):  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Prognostic Marker ◽  
Therapeutic Target ◽  
Dipeptidyl Peptidase ◽  
Dipeptidyl Peptidase Iv ◽  
Papillary Thyroid

Curcumin induces cell death of human papillary thyroid carcinoma BCPAP cells through endoplasmic reticulum stress

RSC Advances ◽  
2016 ◽  
Vol 6 (58) ◽  
pp. 52905-52912 ◽  
Author(s):  
Lixi Zhang ◽  
Li Zhang ◽  
Xian Cheng ◽  
Yanyan Gao ◽  
Jiandong Bao ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Cell Death ◽  
Papillary Thyroid Carcinoma ◽  
Endoplasmic Reticulum Stress ◽  
Thyroid Carcinoma ◽  
Er Stress ◽  
Signaling Pathway ◽  
Papillary Thyroid

Curcumin induced cell death of BCPAP cells via ER stress with activation of the ATF6/XBP-1 signaling pathway and Ca2+ release.

scholarly journals Activated E2F activity induces cell death in papillary thyroid carcinoma K1 cells with enhanced Wnt signaling

PLoS ONE ◽  
2017 ◽  
Vol 12 (6) ◽  
pp. e0178908 ◽  
Author(s):  
Dong Yang ◽  
Chuanjiang Wang ◽  
Yingwei Luo ◽  
Xuan Li ◽  
Qingbin Song ◽  
...  
Keyword(s):  
Cell Death ◽  
Papillary Thyroid Carcinoma ◽  
Thyroid Carcinoma ◽  
Wnt Signaling ◽  
Papillary Thyroid

scholarly journals Vitamin C Cytotoxicity and Its Effects in Redox Homeostasis and Energetic Metabolism in Papillary Thyroid Carcinoma Cell Lines

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 809
Author(s):  
Laura Tronci ◽  
Gabriele Serreli ◽  
Cristina Piras ◽  
Daniela Virginia Frau ◽  
Tinuccia Dettori ◽  
...  
Keyword(s):  
Cell Death ◽  
Papillary Thyroid Carcinoma ◽  
Vitamin C ◽  
Thyroid Carcinoma ◽  
Cell Lines ◽  
Redox Homeostasis ◽  
Tca Cycle ◽  
Genetic Alterations ◽  
High Dose ◽  
Papillary Thyroid

High-dose of vitamin C (L-ascorbic acid, ascorbate) exhibits anti-tumoral effects, primarily mediated by pro-oxidant mechanisms. This cytotoxic effect is thought to affect the reciprocal crosstalk between redox balance and cell metabolism in different cancer types. Vitamin C also inhibits the growth of papillary thyroid carcinoma (PTC) cells, although the metabolic and redox effects remain to be fully understood. To shed light on these aspects, PTC-derived cell lines harboring the most common genetic alterations characterizing this tumor were used. Cell viability, apoptosis, and the metabolome were explored by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide test (MTT), flow cytometry, and UHPLC/MS. Changes were observed in redox homeostasis, with increased reactive oxygen species (ROS) level and perturbation in antioxidants and electron carriers, leading to cell death by both apoptosis and necrosis. The oxidative stress contributed to the metabolic alterations in both glycolysis and TCA cycle. Our results confirm the pro-oxidant effect of vitamin C as relevant in triggering the cytotoxicity in PTC cells and suggest that inhibition of glycolysis and alteration of TCA cycle via NAD+ depletion can play an important role in this mechanism of PTC cancer cell death.

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