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Proposed working model.
Hemin treatment induces ROS and activates NRF2, which lead to the enhanced expression of SESN2. The induction of SESN2 by hemin can be inhibited by the antioxidant NAC and NRF2 inhibitor ML385. In the absence of hemin, SESN2 overexpression leads to reduced oxidative stress and reduced tumor growth, whereas in the presence of hemin, SESN2 overexpression protects cell death and promotes tumor growth.
