Figure 1.

E2 initiates apoptosis through over activation of nuclear ERα. The macromolecule EDC specifically activates non-genomic pathways of ERα mediated by c-Src, which stimulates the proliferation of endocrine-resistant breast cancer cells. In the nucleus, E2 activates classical transcription pathway ERE, which is involved in cellular proliferation. Simultaneously, E2 consistently activates the tethering pathway of ERα, particularly AP-1 family members. This leads to stress responses in the endoplasmic reticulum. Figure republished with permission from AACR (49).