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Proposed model for FoxO3a role in tamoxifen resistant BCCs. The hyper-activated AKT (1) and ERK (2) pathways in TamR cells cause (3) FoxO3a sustained phosphorylation, leading to (4) its proteasomal degradation. (5) The AED LTG restores the response to tamoxifen in TamR BC by inducing FoxO3a. This occurs since LTG, inhibiting the PI3K/Akt pathway (6), re-activates FoxO3a (7), increasing its own transcription (8) [28].
