Peroxiredoxin-1 Tyr194 phosphorylation regulates LOX-dependent extracellular matrix remodelling in breast cancer.


Journal

British journal of cancer
ISSN: 1532-1827
Titre abrégé: Br J Cancer
Pays: England
ID NLM: 0370635

Informations de publication

Date de publication:
10 2021
Historique:
received: 19 01 2021
accepted: 21 07 2021
revised: 22 06 2021
pubmed: 15 8 2021
medline: 18 12 2021
entrez: 14 8 2021
Statut: ppublish

Résumé

Peroxiredoxin 1 (PRDX1) belongs to an abundant family of peroxidases whose role in cancer is still unresolved. While mouse knockout studies demonstrate a tumour suppressive role for PRDX1, in cancer cell xenografts, results denote PRDX1 as a drug target. Probably, this phenotypic discrepancy stems from distinct roles of PRDX1 in certain cell types or stages of tumour progression. We demonstrate an important cell-autonomous function for PRDX1 utilising a syngeneic mouse model (BALB/c) and mammary fibroblasts (MFs) obtained from it. Loss of PRDX1 in vivo promotes collagen remodelling known to promote breast cancer progression. PRDX1 inactivation in MFs occurs via SRC-induced phosphorylation of PRDX1 TYR194 and not through the expected direct oxidation of CYS52 in PRDX1 by ROS. TYR194-phosphorylated PRDX1 fails to bind to lysyl oxidases (LOX) and leads to the accumulation of extracellular LOX proteins which supports enhanced collagen remodelling associated with breast cancer progression. This study reveals a cell type-specific tumour suppressive role for PRDX1 that is supported by survival analyses, depending on PRDX1 protein levels in breast cancer cohorts.

Sections du résumé

BACKGROUND
Peroxiredoxin 1 (PRDX1) belongs to an abundant family of peroxidases whose role in cancer is still unresolved. While mouse knockout studies demonstrate a tumour suppressive role for PRDX1, in cancer cell xenografts, results denote PRDX1 as a drug target. Probably, this phenotypic discrepancy stems from distinct roles of PRDX1 in certain cell types or stages of tumour progression.
METHODS
We demonstrate an important cell-autonomous function for PRDX1 utilising a syngeneic mouse model (BALB/c) and mammary fibroblasts (MFs) obtained from it.
RESULTS
Loss of PRDX1 in vivo promotes collagen remodelling known to promote breast cancer progression. PRDX1 inactivation in MFs occurs via SRC-induced phosphorylation of PRDX1 TYR194 and not through the expected direct oxidation of CYS52 in PRDX1 by ROS. TYR194-phosphorylated PRDX1 fails to bind to lysyl oxidases (LOX) and leads to the accumulation of extracellular LOX proteins which supports enhanced collagen remodelling associated with breast cancer progression.
CONCLUSIONS
This study reveals a cell type-specific tumour suppressive role for PRDX1 that is supported by survival analyses, depending on PRDX1 protein levels in breast cancer cohorts.

Identifiants

pubmed: 34389806
doi: 10.1038/s41416-021-01510-x
pii: 10.1038/s41416-021-01510-x
pmc: PMC8505437
doi:

Substances chimiques

Tyrosine 42HK56048U
Collagen 9007-34-5
PRDX1 protein, human EC 1.11.1.15
Peroxiredoxins EC 1.11.1.15
LOX protein, human EC 1.4.3.13
Protein-Lysine 6-Oxidase EC 1.4.3.13

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1146-1157

Subventions

Organisme : NCI NIH HHS
ID : P30 CA047904
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA131350
Pays : United States
Organisme : NCI NIH HHS
ID : R56 CA233817
Pays : United States

Informations de copyright

© 2021. The Author(s), under exclusive licence to Springer Nature Limited.

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Auteurs

Shireen Attaran (S)

Department of Pharmacology & Chemical Biology, University of Pittsburgh, Pittsburgh, PA, USA.
Women's Cancer Research Center, UPMC Hillman Cancer Center, Pittsburgh, PA, USA.

John J Skoko (JJ)

Department of Pharmacology & Chemical Biology, University of Pittsburgh, Pittsburgh, PA, USA.
Women's Cancer Research Center, UPMC Hillman Cancer Center, Pittsburgh, PA, USA.

Barbara L Hopkins (BL)

Women's Cancer Research Center, UPMC Hillman Cancer Center, Pittsburgh, PA, USA.
Department of Human Genetics, University of Pittsburgh, Pittsburgh, PA, USA.

Megan K Wright (MK)

University of Pittsburgh, School of Medicine, Pittsburgh, PA, USA.

Laurel E Wood (LE)

Department of Pharmacology & Chemical Biology, University of Pittsburgh, Pittsburgh, PA, USA.

Alparslan Asan (A)

Department of Pharmacology & Chemical Biology, University of Pittsburgh, Pittsburgh, PA, USA.
Women's Cancer Research Center, UPMC Hillman Cancer Center, Pittsburgh, PA, USA.

Hyun Ae Woo (HA)

College of Pharmacy, Graduate School of Pharmaceutical Sciences, Ewha Womans University, Seoul, Republic of Korea.

Adam Feinberg (A)

Department of Materials Science and Engineering and Biomedical Engineering, Carnegie Mellon University, Pittsburgh, PA, USA.

Carola A Neumann (CA)

Department of Pharmacology & Chemical Biology, University of Pittsburgh, Pittsburgh, PA, USA. neumannc@upmc.edu.
Women's Cancer Research Center, UPMC Hillman Cancer Center, Pittsburgh, PA, USA. neumannc@upmc.edu.

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