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. Author manuscript; available in PMC: 2020 Jan 1.
Published in final edited form as: Semin Radiat Oncol. 2019 Jan;29(1):42–54. doi: 10.1016/j.semradonc.2018.10.003

Figure 3. NRF2 acts as a central hub to facilitate the transition of BCSCs from the M to E state as well as the maintenance/proliferation of E-BCSCs under metabolic/oxidant stress.

Figure 3.

The activation of NRF2 during metabolic/oxidant stress promotes CSC plasticity by mediating AMPK-dependent HIF1α stabilization, which is required for the conversion of M- to E-BCSCs. NRF2 activation also mediates the activation of HIF1α-NOTCH self-renewal pathway and the expression of NRF2 target genes ALDH1A1/3 to facilitate the propagation of E-BCSCs.