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HAX1 is a novel binding partner of Che-1/AATF. Implications in oxidative stress cell response.

Authors :
Pisani C
Onori A
Gabanella F
Iezzi S
De Angelis R
Fanciulli M
Colizza A
de Vincentiis M
Di Certo MG
Passananti C
Corbi N
Source :
Biochimica et biophysica acta. Molecular cell research [Biochim Biophys Acta Mol Cell Res] 2024 Jan; Vol. 1871 (1), pp. 119587. Date of Electronic Publication: 2023 Sep 22.
Publication Year :
2024

Abstract

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 (ERĪ±) upon H <subscript>2</subscript> O <subscript>2</subscript> treatment. These results indicate the two anti-apoptotic proteins HAX1 and Che-1 as coordinated players in cellular response to oxidative stress with a potential role in estrogen sensitive breast cancer cells.<br />Competing Interests: 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.<br /> (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)

Details

Language :
English
ISSN :
1879-2596
Volume :
1871
Issue :
1
Database :
MEDLINE
Journal :
Biochimica et biophysica acta. Molecular cell research
Publication Type :
Academic Journal
Accession number :
37742722
Full Text :
https://doi.org/10.1016/j.bbamcr.2023.119587