Heme Oxygenase Modulation Drives Ferroptosis in TNBC Cells.
HO-1
HO-2
cancer
curcumin
erastin
heme
inducers
inhibitors
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
20 May 2022
20 May 2022
Historique:
received:
26
04
2022
revised:
17
05
2022
accepted:
19
05
2022
entrez:
28
5
2022
pubmed:
29
5
2022
medline:
1
6
2022
Statut:
epublish
Résumé
The term ferroptosis refers to a peculiar type of programmed cell death (PCD) mainly characterized by extensive iron-dependent lipid peroxidation. Recently, ferroptosis has been suggested as a potential new strategy for the treatment of several cancers, including breast cancer (BC). In particular, among the BC subtypes, triple negative breast cancer (TNBC) is considered the most aggressive, and conventional drugs fail to provide long-term efficacy. In this context, our study's purpose was to investigate the mechanism of ferroptosis in breast cancer cell lines and reveal the significance of heme oxygenase (HO) modulation in the process, providing new biochemical approaches. HO's effect on BC was evaluated by MTT tests, gene silencing, Western blot analysis, and measurement of reactive oxygen species (ROS), glutathione (GSH) and lipid hydroperoxide (LOOH) levels. In order to assess HO's implication, different approaches were exploited, using two distinct HO-1 inducers (hemin and curcumin), a well-known HO inhibitor (SnMP) and a selective HO-2 inhibitor. The data obtained showed HO's contribution to the onset of ferroptosis; in particular, HO-1 induction seemed to accelerate the process. Moreover, our results suggest a potential role of HO-2 in erastin-induced ferroptosis. In view of the above, HO modulation in ferroptosis can offer a novel approach for breast cancer treatment.
Identifiants
pubmed: 35628518
pii: ijms23105709
doi: 10.3390/ijms23105709
pmc: PMC9143660
pii:
doi:
Substances chimiques
Lipid Peroxides
0
Reactive Oxygen Species
0
Heme Oxygenase (Decyclizing)
EC 1.14.14.18
Glutathione
GAN16C9B8O
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : This work was founded by the University of Catania, Programma Ricerca di Ateneo Pia.Ce.Ri 2020-2022 linea 2
ID : project number 57722172126
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