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Epithelial-Mesenchymal transition induces podocalyxin to promote extravasation via ezrin signaling

The epithelial-mesenchymal transition (EMT) endows carcinoma cells with traits needed to complete many of the steps leading to metastasis formation, but its contributions specifically to the late step of extravasation remain understudied. We find that breast cancer cells that have undergone an EMT e...

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Main Authors: Fröse, Julia (Author) , Chen, Michelle B. (Author) , Hebron, Katie E. (Author) , Reinhardt, Ferenc (Author) , Hajal, Cynthia (Author) , Zijlstra, Andries (Author) , Kamm, Roger D. (Author) , Weinberg, Robert A. (Author)
Format: Article (Journal)
Language:English
Published: 24 July 2018
In: Cell reports
Year: 2018, Volume: 24, Issue: 4, Pages: 962-972
ISSN:2211-1247
DOI:10.1016/j.celrep.2018.06.092
Online Access:Verlag, Volltext: https://doi.org/10.1016/j.celrep.2018.06.092
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Author Notes:Julia Fröse, Michelle B. Chen, Katie E. Hebron, Ferenc Reinhardt, Cynthia Hajal, Andries Zijlstra, Roger D. Kamm, and Robert A. Weinberg

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520 |a The epithelial-mesenchymal transition (EMT) endows carcinoma cells with traits needed to complete many of the steps leading to metastasis formation, but its contributions specifically to the late step of extravasation remain understudied. We find that breast cancer cells that have undergone an EMT extravasate more efficiently from blood vessels both in vitro and in vivo. Analysis of gene expression changes associated with the EMT program led to the identification of an EMT-induced cell-surface protein, podocalyxin (PODXL), as a key mediator of extravasation in mesenchymal breast and pancreatic carcinoma cells. PODXL promotes extravasation through direct interaction of its intracellular domain with the cytoskeletal linker protein ezrin. Ezrin proceeds to establish dorsal cortical polarity, enabling the transition of cancer cells from a non-polarized, rounded cell morphology to an invasive extravasation-competent shape. Hence, the EMT program can directly enhance the efficiency of extravasation and subsequent metastasis formation through a PODXL-ezrin signaling axis. 
650 4 |a Animals 
650 4 |a Breast Neoplasms 
650 4 |a Cell Line, Tumor 
650 4 |a Cytoskeletal Proteins 
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650 4 |a extravasation 
650 4 |a ezrin 
650 4 |a Female 
650 4 |a Heterografts 
650 4 |a Humans 
650 4 |a Lung Neoplasms 
650 4 |a Male 
650 4 |a metastasis 
650 4 |a Mice 
650 4 |a Mice, Inbred NOD 
650 4 |a Mice, SCID 
650 4 |a Pancreatic Neoplasms 
650 4 |a PODXL 
650 4 |a Sialoglycoproteins 
650 4 |a Signal Transduction 
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