Fig 3.

Proposed model for ERα-dependent KP/KISS1R signaling in breast epithelia. In normal healthy mammary epithelia, estrogen signaling through ERα is responsible for maintaining normal breast epithelial growth and function, keeping KP/KISS1R signaling in check through transcriptional regulation of KISS and/or KISS1R. However, in breast cancer, when ERα expression is lost or silenced, this results in increased transcription of KISS1 and/or KISS1R, and increased receptor signaling and the induction of EMT, allowing epithelial cells to acquire a more migratory and invasive phenotype.