Ferroptosis vulnerability in MYCN‐driven neuroblastomas.

Resistance to cell death is an important hallmark of cancer.1 Over the past two decades, researchers have been developing therapeutic strategies to target cell death signalling pathways for cancer treatment. Likewise, CTH inhibition exerted more ferroptosis-sensitizing effects on MYCN-high adrenergic neuroblastoma cells than on MYCN-high mesenchymal neuroblastoma cells. Further studies by the authors suggested that, in MYCN-high adrenergic neuroblastoma cells, upregulated transsulfuration pathway maintains the source of intracellular cysteine for protein synthesis at the expense of GSH synthesis, thus triggering a ferroptosis vulnerability. [Extracted from the article]