Glucose and Inositol Transporters, SLC5A1 and SLC5A3, in Glioblastoma Cell Migration.

phlorizin transportome volume regulation

Journal

Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829

Informations de publication

Date de publication:
24 Nov 2022
Historique:
received: 06 10 2022
revised: 04 11 2022
accepted: 20 11 2022
entrez: 11 12 2022
pubmed: 12 12 2022
medline: 12 12 2022
Statut: epublish

Résumé

(1) Background: The recurrence of glioblastoma multiforme (GBM) is mainly due to invasion of the surrounding brain tissue, where organic solutes, including glucose and inositol, are abundant. Invasive cell migration has been linked to the aberrant expression of transmembrane solute-linked carriers (SLC). Here, we explore the role of glucose (SLC5A1) and inositol transporters (SLC5A3) in GBM cell migration. (2) Methods: Using immunofluorescence microscopy, we visualized the subcellular localization of SLC5A1 and SLC5A3 in two highly motile human GBM cell lines. We also employed wound-healing assays to examine the effect of SLC inhibition on GBM cell migration and examined the chemotactic potential of inositol. (3) Results: While GBM cell migration was significantly increased by extracellular inositol and glucose, it was strongly impaired by SLC transporter inhibition. In the GBM cell monolayers, both SLCs were exclusively detected in the migrating cells at the monolayer edge. In single GBM cells, both transporters were primarily localized at the leading edge of the lamellipodium. Interestingly, in GBM cells migrating via blebbing, SLC5A1 and SLC5A3 were predominantly detected in nascent and mature blebs, respectively. (4) Conclusion: We provide several lines of evidence for the involvement of SLC5A1 and SLC5A3 in GBM cell migration, thereby complementing the migration-associated transportome. Our findings suggest that SLC inhibition is a promising approach to GBM treatment.

Identifiants

pubmed: 36497276
pii: cancers14235794
doi: 10.3390/cancers14235794
pmc: PMC9738886
pii:
doi:

Types de publication

Journal Article

Langues

eng

Commentaires et corrections

Type : ErratumIn

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Auteurs

Philippa K Brosch (PK)

Department of Biotechnology & Biophysics, Biocenter, University of Würzburg, 97074 Würzburg, Germany.

Tessa Korsa (T)

Department of Biotechnology & Biophysics, Biocenter, University of Würzburg, 97074 Würzburg, Germany.
Fraunhofer Institute for Biomedical Engineering (IBMT), 66280 Sulzbach, Germany.

Danush Taban (D)

Department of Biotechnology & Biophysics, Biocenter, University of Würzburg, 97074 Würzburg, Germany.

Patrick Eiring (P)

Department of Biotechnology & Biophysics, Biocenter, University of Würzburg, 97074 Würzburg, Germany.

Sascha Hildebrand (S)

Department of Biotechnology & Biophysics, Biocenter, University of Würzburg, 97074 Würzburg, Germany.

Julia Neubauer (J)

Fraunhofer Institute for Biomedical Engineering (IBMT), 66280 Sulzbach, Germany.

Heiko Zimmermann (H)

Fraunhofer Institute for Biomedical Engineering (IBMT), 66280 Sulzbach, Germany.
Department of Molecular and Cellular Biotechnology, Saarland University, 66123 Saarbrücken, Germany.
Faculty of Marine Science, Universidad Católica del Norte, Coquimbo 1281, Chile.

Markus Sauer (M)

Department of Biotechnology & Biophysics, Biocenter, University of Würzburg, 97074 Würzburg, Germany.

Ryo Shirakashi (R)

Institute of Industrial Science, The University of Tokyo, Tokyo 153-8505, Japan.

Cholpon S Djuzenova (CS)

Department of Radiation Oncology, University Hospital of Würzburg, 97080 Würzburg, Germany.

Dmitri Sisario (D)

Department of Biotechnology & Biophysics, Biocenter, University of Würzburg, 97074 Würzburg, Germany.

Vladimir L Sukhorukov (VL)

Department of Biotechnology & Biophysics, Biocenter, University of Würzburg, 97074 Würzburg, Germany.

Classifications MeSH