scholarly journals Change in cell shape is required for matrix metalloproteinase-induced epithelial-mesenchymal transition of mammary epithelial cells

2008 ◽  
Vol 105 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Celeste M. Nelson ◽  
Davitte Khauv ◽  
Mina J. Bissell ◽  
Derek C. Radisky
Keyword(s):  
Epithelial Cells ◽  
Matrix Metalloproteinase ◽  
Cell Shape ◽  
Epithelial Mesenchymal Transition ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Mesenchymal Transition

Extracellular vesicles from women with breast cancer promote an epithelial-mesenchymal transition-like process in mammary epithelial cells MCF10A

Tumor Biology ◽  
2015 ◽  
Vol 36 (12) ◽  
pp. 9649-9659 ◽  
Author(s):  
Octavio Galindo-Hernandez ◽  
Cristina Gonzales-Vazquez ◽  
Pedro Cortes-Reynosa ◽  
Emmanuel Reyes-Uribe ◽  
Sonia Chavez-Ocaña ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Epithelial Cells ◽  
Extracellular Vesicles ◽  
Epithelial Mesenchymal Transition ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Mesenchymal Transition

scholarly journals Upregulated-flotillins and sphingosine kinase 2 derail vesicular trafic to stabilize AXL and promote epithelial-mesenchymal transition

2020 ◽  
Author(s):  
Mallory Genest ◽  
Franck Comunale ◽  
Damien Planchon ◽  
Pauline Govindin ◽  
Sophie Vacher ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Epithelial Mesenchymal Transition ◽  
Mammary Epithelial Cells ◽  
Sphingosine Kinase ◽  
Vesicular Trafficking ◽  
Mammary Epithelial ◽  
Lipid Kinase ◽  
Mesenchymal Transition ◽  
Sphingosine Kinase 2

AbstractAltered endocytosis and vesicular trafficking are major players during tumorigenesis. Flotillin overexpression, a feature observed in many invasive tumors, and identified as a marker of poor prognosis, induces a deregulated endocytic and trafficking pathway called Upregulated Flotillin-Induced Trafficking (UFIT). Here, we found that, in non tumoral mammary epithelial cells, induction of the UFIT pathway promotes epithelial-to-mesenchymal transition (EMT) and accelerates the endocytosis of several transmembrane receptors, including AXL, in flotillin-positive late endosomes. AXL overexpression, frequently observed in cancer cells, is linked to EMT and metastasis formation. In flotillin-overexpressing non-tumoral mammary epithelial cells and in invasive breast carcinoma cells, we found that the UFIT-mediated AXL endocytosis allows its stabilization and depends on sphingosine-kinase 2, a lipid kinase recruited in flotillin-rich plasma membrane-domains and endosomes.Thus, the deregulation of vesicular trafficking following flotillin upregulation, and through sphingosine kinase 2, emerges as a new mechanism of AXL overexpression and EMT-inducing signaling pathway activation.

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