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![Transcriptional coactivator MED1 in the interface of anti-estrogen and anti-HER2 therapeutic resistance](https://image.oaes.cc/23963ef2-37db-4c3c-abb4-fa0f268930a7/4752.fig.2.jpg)
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.