Transforming growth factor-β1, β2, and β3, urokinase and parathyroid hormone-related peptide expression in 8701-BC breast cancer cells and clones

1993 ◽  
Vol 55 (1) ◽  
pp. 73-80 ◽  
Author(s):  
Claudio Luparello ◽  
Andrew F. Ginty ◽  
James A. Gallagher ◽  
Ida Pucci-Minafra ◽  
Salvatore Minafra
2009 ◽  
Vol 108 (2) ◽  
pp. 408-414 ◽  
Author(s):  
Sukyee Kwok ◽  
Susan R. Rittling ◽  
Nicola C. Partridge ◽  
Chellakkan S. Benson ◽  
Mayuranathan Thiyagaraj ◽  
...  

Cancers ◽  
2018 ◽  
Vol 10 (7) ◽  
pp. 234 ◽  
Author(s):  
Mariafrancesca Cascione ◽  
Valeria De Matteis ◽  
Chiara Toma ◽  
Stefano Leporatti

The Epithelial to mesenchymal transition (EMT) is the process that drives epithelial tumor cells to acquire an invasive phenotype. The role of transforming growth factor-β1 (TGF-β1) in EMT is still debated. We used confocal laser scanning microscopy and scanning force spectroscopy to perform a morphomechanical analysis on epithelial breast cancer cells (MCF-7), comparing them before and after TGF-β1 exogenous stimulation (5 ng/mL for 48 h). After TGF-β1 treatment, loss of cell–cell adherence (mainly due to the reduction of E-cadherin expression of about 24%) and disaggregation of actin cortical fibers were observed in treated MCF-7. In addition, TGF-β1 induced an alteration of MCF-7 nuclei morphology as well as a decrease in the Young’s modulus, owing to a rearrangement that involved the cytoskeletal networks and the nuclear region. These relevant variations in morphological features and mechanical properties, elicited by TGF-β1, suggested an increased capacity of MCF-7 to migrate, which was confirmed by a wound healing assay. By means of our biophysical approach, we highlighted the malignant progression of breast cancer cells induced by TGF-β1 exposure. We are confirming TGF-β1’s role in EMT by means of morphomechanical evidence that could represent a turning point in understanding the molecular mechanisms involved in cancer progression.


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