Fig. 8: Selective inhibition of Nrf2 and autophagy due to SeC in Nrf2-addicted CRC cells. | Cell Death & Disease

Fig. 8: Selective inhibition of Nrf2 and autophagy due to SeC in Nrf2-addicted CRC cells.

From: Blockage of Nrf2 and autophagy by L-selenocystine induces selective death in Nrf2-addicted colorectal cancer cells through p62-Keap-1-Nrf2 axis

Fig. 8

In non–Nrf2-addicted cells, SeC induced slightly low ROS levels and then effectively triggered Nrf2 and autophagy activations. The autophagic proteins, such as ULK1 and LC3II, increased in the SeC-treated non-Nrf2-addicted cells. SeC induced Nrf2 activation and translocation, resulting in NQO1 and HO-1 increasing in the non–Nrf2-addicted cells. Therefore, the ROS was below the threshold level and no cell death occurred. By contrast, SeC induced ROS prodiction and inhibited the Nrf2 and autophagy pathways in Nrf2-addicted cells. The antioxidative enzymes xCT and NQO1 were decreased by SeC. SeC inhibits Nrf2 activation, which may lead to anoverwhelming ROS accumulation, subsequently triggering cell death. P phosphorylation.

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