fig2

Figure 2. Molecular mechanisms of HER2 and MED1 in anti-estrogen treatment resistance. In endocrine-sensitive breast cancer cells, treatment with anti-estrogen tamoxifen results in the recruitment of co-repressors to suppress gene transcription. However, when MED1 is overexpressed and phosphorylated by growth factor cascades such as HER2, the MED1/Mediator complex rather than ER co-repressors is recruited to activate gene transcription and render endocrine resistance. Adapted from Leonard et al.^[72], JZUS-B.