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. Author manuscript; available in PMC: 2017 Jul 1.
Published in final edited form as: J Steroid Biochem Mol Biol. 2015 Aug 13;161:73–83. doi: 10.1016/j.jsbmb.2015.07.018

Figure 1. Three mechanisms of ER genomic signaling and the inhibition by antiestrogens and aromatase inhibitors.

Figure 1

Testosterone (T) is converted into estrogen (E2) by the enzyme aromatase. Normal breast cells synthesize E2 which has autocrine and paracrine functions. Breast cancer cells express higher levels of aromatase; thus, their E2 concentration is higher than normal breast cell. Furthermore, ER-positive breast cells require E2 for growth and utilize certain genomic signaling pathways to transcribe ER-regulated genes. These pathways include: classical genomic (E2-ER complex binds to the ERE); ERE-independent genomic (E2-ER complex binds to transcription factor-TF-binding sites); and non-classical genomic (ER is phosphorylated in absence of E2 via kinase cascades).