Fig 2.

Novel KP/KISS1R signaling pathways in breast cancer cells lacking the estrogen receptor, ERα. ERα has been found to negatively regulates KISS1R expression. KISS1R activation in these cells leads to epidermal growth factor (EGFR) transactivation via β-arrestin 2- and IQGAP1-mediated pathways. KISS1R activation can induce epithelial-mesenchymal transition (EMT), resulting in a decrease in E-cadherin expression and acquisition of a mesenchymal phenotype, characterized by actin cytoskeleton re-organization and stress fiber formation. Expression of mesenchymal markers (Snail/slug, N-cadherin, Vimentin) also increases. KP/KISS1R pathway can also activate RhoA. Blue solid lines represent KISS1R interacting proteins; black dashed lines represent EGFR interacting proteins.