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Updated: Jun 27, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Prolactin-induced tyrosyl phosphorylation of PAK1 facilitates epithelial-mesenchymal transition
Alan Hammer1, Maria Diakonova1
1Department of Biological Sciences, University of Toledo, Toledo, Ohio, United States.
Abstract:
PAK1 and prolactin (PRL) regulate breast cancer. Prolactin-activated JAK2 tyrosyl phosphorylates PAK1 (pTyr-PAK1). We demonstrate here that pTyr-PAK1 regulates epithelial-mesenchymal transition (EMT) in breast cancer cells. PRL treatment of T47D PAK1 WT cells leads to downregulation of E-cadherin surface expression and "ectodomain shedding" (extracellular cleavage of E-cadherin). pTyr-PAK1 increases mRNA levels of Snail, Slug, and Twist2, transcriptional factors implicated in E-cadherin repression. pTyr-PAK1 also significantly increases PRL-dependent Slug activity leading to expression of vimentin, a hallmark of EMT. Thus, our current data on pTyr-PAK1 regulation of EMT bring insight into the role of PAK1 and PRL in human breast cancer.
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