Abstract
Hormones estrogen and prolactin exert independent effects on breast cancer while their crosstalk synergistically enhance breast cancer cell proliferation. We have previously shown that the serine/threonine kinase PAK1 is responsible for this effect and proposed the mechanism of PAK1 action. Here we extended our previous data to demonstrate that the PAK1 kinase is a common interplay in PRL and E2 crosstalk to regulate epithelial-mesenchymal transition, cell migration and invasiveness of human breast cancer cells.
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