Neuroblastoma response to RAS-MAPK inhibitors and APR-246 (eprenetapopt) co-treatment is dependent on SLC7A11.

ABSTRACT:

Background

We previously demonstrated that APR-246 (eprenetapopt) could be an efficient treatment option against neuroblastoma (NB), the most common pediatric extracranial solid tumor. APR-246's mechanism of action is not completely understood and can differ between cell types. Here we investigate the involvement of well-known oncogenic pathways in NB's response to APR-246.

Methods

A proteome profiler kinase assays and western blot analysis were used to identify the molecular pathways involved in the responses to APR-246. Bulk ATP levels were used to determine the viability of cells and the IC₅₀ for APR-246. Cystine-FITC was used to measure the cellular uptake of cysteine. PmRNA5 was used to activate ERK1/2 and pshRNA1 was used to silence HSP27. An IMR-32 xenograf

SUBMITTER: Mlakar V 

PROVIDER: S-EPMC11664348 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature