NQO1 plays critical roles at both the cell-autonomous and cell-extrinsic levels for clinical treatment. Targeting NQO1 and its downstream signaling pathways, including β-Lapachone and immune checkpoint inhibitors such as anti-PD-1 therapy, enhances our understanding of the interactions between GSCs, oxidative stress, and the TME. This offers promising new avenues for clinical intervention in GBM.
Li et al. (Thu,) studied this question.