Fig. 3: Nrf2 inhibitor enhances the sensitivity of CRC cells to the ferroptosis induced by RSL3 or Erastin. | Cell Death & Disease

Fig. 3: Nrf2 inhibitor enhances the sensitivity of CRC cells to the ferroptosis induced by RSL3 or Erastin.

From: RETRACTED ARTICLE: Ibrutinib facilitates the sensitivity of colorectal cancer cells to ferroptosis through BTK/NRF2 pathway

Fig. 3

HT-29 cells were treated with RSL3 or Erastin with or without the presence of Nrf2 inhibitor, NRF2-IN-1. The cell (A) viability and (B) proliferation were assessed via the CCK-8 assay and the colony formation assay. The C MDA and D GSH levels were detected in HT-29 cells that were treated with RSL3 or Erastin with or without the presence of Nrf2 inhibitor, NRF2-IN-1. E The representative immunofluorescent staining images of Nrf2 in HT-29 cells that were treated with RSL3 or Erastin with or without the presence of Nrf2 inhibitor, NRF2-IN-1. Scale bar = 25 μm. F The Nrf2, GPX4, SOD1, and CAT expressions in HT-29 cells that were treated with RSL3 or Erastin with or without the presence of Nrf2 inhibitor, NRF2-IN-1. Caco-2 cells were treated with RSL3 or Erastin with or without the presence of Nrf2 promotor, TAT-14. The cell G viability and H proliferation were assessed via the CCK-8 assay and the colony formation assay. The I MDA and J GSH levels were detected in Caco-2 cells that were treated with RSL3 or Erastin with or without the presence of Nrf2 promotor, TAT-14. K The representative immunofluorescent staining images of Nrf2 in Caco-2 cells that were treated with RSL3 or Erastin with or without the presence of Nrf2 promotor, TAT-14. Scale bar = 25 μm. L The Nrf2, GPX4, SOD1, and CAT expressions in Caco-2 cells that were treated with RSL3 or Erastin with or without the presence of Nrf2 promotor, TAT-14. All experiments were carried out at least three times, n = 3, *P < 0.05, **P < 0.01, and ***P < 0.001.

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