Neuroblastoma response to RAS-MAPK inhibitors and APR-246 (eprenetapopt) co-treatment is dependent on SLC7A11
These results demonstrated a pivotal role of the RAS-MAPK pathway in the NB cellular response to APR-246 via the modulation of intracellular concentrations of GSH and the transport of cystine through SLC7A11, phosphorylation of Hsp27, and programmed cell death. Combining APR-246 with RAS-MAPK pathway inhibitors can, in some cases, lead to antagonistic action, which can be reversed by combining APR-246 with the clinically approved drug sulfasalazine.
Authors
- Ina Oehme (ORCID: https://orcid.org/0000-0002-0827-2356)
- Fabienne Gumy‐Pause (ORCID: https://orcid.org/0000-0002-2835-4367)
- Vid Mlakar (ORCID: https://orcid.org/0000-0003-4968-5592)
- Laurence Lesne
- Sara Najafi (ORCID: https://orcid.org/0000-0003-1218-1817)
- Marc Ansari (ORCID: https://orcid.org/0000-0002-9649-6498)
Institutions
- University of Geneva (CH)
- German Cancer Research Center (DE)
- Heidelberg University (DE)
- University Hospital Heidelberg (DE)
- University Hospital of Geneva (CH)
- Hopp Children's Cancer Center Heidelberg (DE)
- Deutsches Konsortium für Translationale Krebsforschung (DE)
Publication Details
- Journal
- Frontiers in Oncology
- Published
- 2024-12-06
- DOI
- https://doi.org/10.3389/fonc.2024.1433256
- Citations
- 2
- Primary Topic
- Neuroblastoma Research and Treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.74