Loss of pro-apoptotic Bax and Bak increases resistance to dihydroartemisinin-mediated cytotoxicity in normoxia but not in hypoxia in HCT116 colorectal cancer cells.
Apoptosis
Dihydroartemisinin
Glutathione
Hypoxia
Lipid peroxidation
Reactive oxygen species
Therapy resistance
Journal
Free radical biology & medicine
ISSN: 1873-4596
Titre abrégé: Free Radic Biol Med
Pays: United States
ID NLM: 8709159
Informations de publication
Date de publication:
10 2021
10 2021
Historique:
received:
14
05
2021
revised:
04
08
2021
accepted:
12
08
2021
pubmed:
18
8
2021
medline:
10
9
2021
entrez:
17
8
2021
Statut:
ppublish
Résumé
Tumor hypoxia is a major biological factor that drives resistance to chemotherapy and radiotherapy. We previously demonstrated that the pro-oxidative drug dihydroartemisinin (DHA) efficiently targeted normoxic and hypoxic cancer cells. Although well studied in normoxia, the mechanism behind DHA-mediated cytotoxicity in hypoxia is insufficiently explored. Here, we analyzed the effect of DHA in HCT116 wild type (wt) cells and in HCT116 Bax
Identifiants
pubmed: 34403740
pii: S0891-5849(21)00471-8
doi: 10.1016/j.freeradbiomed.2021.08.012
pii:
doi:
Substances chimiques
Artemisinins
0
bcl-2-Associated X Protein
0
artenimol
6A9O50735X
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
157-170Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.