HAX1 is a novel binding partner of Che-1/AATF. Implications in oxidative stress cell response.
Apoptosis
Breast cancer
ERα
HAX1
Mitochondria
Oxidative stress
Journal
Biochimica et biophysica acta. Molecular cell research
ISSN: 1879-2596
Titre abrégé: Biochim Biophys Acta Mol Cell Res
Pays: Netherlands
ID NLM: 101731731
Informations de publication
Date de publication:
01 2024
01 2024
Historique:
received:
18
05
2023
revised:
31
08
2023
accepted:
14
09
2023
medline:
20
11
2023
pubmed:
25
9
2023
entrez:
24
9
2023
Statut:
ppublish
Résumé
HAX1 is a multifunctional protein involved in the antagonism of apoptosis in cellular response to oxidative stress. In the present study we identified HAX1 as a novel binding partner for Che-1/AATF, a pro-survival factor which plays a crucial role in fundamental processes, including response to multiple stresses and apoptosis. HAX1 and Che-1 proteins show extensive colocalization in mitochondria and we demonstrated that their association is strengthened after oxidative stress stimuli. Interestingly, in MCF-7 cells, resembling luminal estrogen receptor (ER) positive breast cancer, we found that Che-1 depletion correlates with decreased HAX1 mRNA and protein levels, and this event is not significantly affected by oxidative stress induction. Furthermore, we observed an enhancement of the previously reported interaction between HAX1 and estrogen receptor alpha (ERα) upon H
Identifiants
pubmed: 37742722
pii: S0167-4889(23)00160-X
doi: 10.1016/j.bbamcr.2023.119587
pii:
doi:
Substances chimiques
Hydrogen Peroxide
BBX060AN9V
Apoptosis Regulatory Proteins
0
AATF protein, human
0
Repressor Proteins
0
HAX1 protein, human
0
Adaptor Proteins, Signal Transducing
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
119587Informations de copyright
Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.