Altered Regulation of the Glucose Transporter GLUT3 in PRDX1 Null Cells Caused Hypersensitivity to Arsenite.

GLUT3 redox state PRDX1 SLC2A3 arsenite sensitivity

Journal

Cells
ISSN: 2073-4409
Titre abrégé: Cells
Pays: Switzerland
ID NLM: 101600052

Informations de publication

Date de publication:
22 Nov 2023
Historique:
received: 09 10 2023
revised: 13 11 2023
accepted: 18 11 2023
medline: 9 12 2023
pubmed: 9 12 2023
entrez: 9 12 2023
Statut: epublish

Résumé

Targeting tumour metabolism through glucose transporters is an attractive approach. However, the role these transporters play through interaction with other signalling proteins is not yet defined. The glucose transporter SLC2A3 (GLUT3) is a member of the solute carrier transporter proteins. GLUT3 has a high affinity for D-glucose and regulates glucose uptake in the neurons, as well as other tissues. Herein, we show that GLUT3 is involved in the uptake of arsenite, and its level is regulated by peroxiredoxin 1 (PRDX1). In the absence of PRDX1, GLUT3 mRNA and protein expression levels are low, but they are increased upon arsenite treatment, correlating with an increased uptake of glucose. The downregulation of GLUT3 by siRNA or deletion of the gene by CRISPR cas-9 confers resistance to arsenite. Additionally, the overexpression of GLUT3 sensitises the cells to arsenite. We further show that GLUT3 interacts with PRDX1, and it forms nuclear foci, which are redistributed upon arsenite exposure, as revealed by immunofluorescence analysis. We propose that GLUT3 plays a role in mediating the uptake of arsenite into cells, and its homeostatic and redox states are tightly regulated by PRDX1. As such, GLUT3 and PRDX1 are likely to be novel targets for arsenite-based cancer therapy.

Identifiants

pubmed: 38067110
pii: cells12232682
doi: 10.3390/cells12232682
pmc: PMC10705171
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

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Auteurs

Reem Ali (R)

College of Health and Life Sciences, Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), Education City, Doha 34110, Qatar.

Abdallah Alhaj Sulaiman (A)

College of Health and Life Sciences, Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), Education City, Doha 34110, Qatar.

Bushra Memon (B)

College of Health and Life Sciences, Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), Education City, Doha 34110, Qatar.
Diabetes Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), Doha 34110, Qatar.

Singdhendubala Pradhan (S)

Division of Sustainable Development, College of Science and Engineering, Hamad Bin Khalifa University, Doha 34110, Qatar.

Mashael Algethami (M)

Nottingham Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.

Mustapha Aouida (M)

College of Health and Life Sciences, Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), Education City, Doha 34110, Qatar.

Gordon McKay (G)

Division of Sustainable Development, College of Science and Engineering, Hamad Bin Khalifa University, Doha 34110, Qatar.

Srinivasan Madhusudan (S)

Nottingham Biodiscovery Institute, School of Medicine, University of Nottingham, University Park, Nottingham NG7 3RD, UK.
Department of Oncology, Nottingham University Hospitals, Nottingham NG5 1PB, UK.

Essam M Abdelalim (EM)

College of Health and Life Sciences, Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), Education City, Doha 34110, Qatar.
Diabetes Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), Doha 34110, Qatar.

Dindial Ramotar (D)

College of Health and Life Sciences, Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), Education City, Doha 34110, Qatar.

Classifications MeSH