Targeting the pentose phosphate pathway increases reactive oxygen species and induces apoptosis in thyroid cancer cells.


Journal

Molecular and cellular endocrinology
ISSN: 1872-8057
Titre abrégé: Mol Cell Endocrinol
Pays: Ireland
ID NLM: 7500844

Informations de publication

Date de publication:
01 01 2020
Historique:
received: 28 04 2019
revised: 24 09 2019
accepted: 24 09 2019
pubmed: 30 9 2019
medline: 21 10 2020
entrez: 30 9 2019
Statut: ppublish

Résumé

The pentose phosphate pathway (PPP) plays an important role in the biosynthesis of ribonucleotide precursor and NADPH. Cancer cells frequently increase the flux of glucose into the PPP to support the anabolic demands and regulate oxidative stress. Consistently, metabolomic analyses indicate an upregulation of the PPP in thyroid cancer. In the present study, we found that the combination of glucose-6-phosphate dehydrogenase (G6PD) and transketolase inhibitors (6-aminonicotinamide and oxythiamine) exerted an additive or synergistic effect on cell growth inhibition in thyroid cancer cells. Targeting PPP significantly increased cellular reactive oxygen species (ROS) and induced endoplasmic reticulum (ER) stress and apoptosis. Suppressed cell viability could be partially rescued with treatment with the ROS scavenger or apoptosis inhibitor but not ER-stress inhibitor. Taken together, dual PPP blockade leads to pharmacologic additivity or synergism and causes ROS-mediated apoptosis in thyroid cancer cells.

Identifiants

pubmed: 31563469
pii: S0303-7207(19)30297-7
doi: 10.1016/j.mce.2019.110595
pii:
doi:

Substances chimiques

Reactive Oxygen Species 0
Oxythiamine 136-16-3
6-Aminonicotinamide 329-89-5
NADP 53-59-8
Glucosephosphate Dehydrogenase EC 1.1.1.49

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

110595

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Chien-Liang Liu (CL)

Department of Surgery, MacKay Memorial Hospital and Mackay Medical College, Taipei, Taiwan, ROC; Department of Medical Research, MacKay Memorial Hospital, Taipei, Taiwan, ROC.

Yi-Chiung Hsu (YC)

Department of Biomedical Sciences and Engineering, National Central University, Taoyuan City,Taiwan, ROC.

Jie-Jen Lee (JJ)

Department of Surgery, MacKay Memorial Hospital and Mackay Medical College, Taipei, Taiwan, ROC.

Ming-Jen Chen (MJ)

Department of Surgery, MacKay Memorial Hospital and Mackay Medical College, Taipei, Taiwan, ROC; Department of Medical Research, MacKay Memorial Hospital, Taipei, Taiwan, ROC.

Chi-Hsin Lin (CH)

Department of Medical Research, MacKay Memorial Hospital, Taipei, Taiwan, ROC; Department of Bioscience Technology, Chung Yuan Christian University, Taoyuan City, Taiwan, ROC.

Shih-Yuan Huang (SY)

Department of Medical Research, MacKay Memorial Hospital, Taipei, Taiwan, ROC.

Shih-Ping Cheng (SP)

Department of Surgery, MacKay Memorial Hospital and Mackay Medical College, Taipei, Taiwan, ROC; Department of Pharmacology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan, ROC. Electronic address: surg.mmh@gmail.com.

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Classifications MeSH