scholarly journals Controlled Extracellular Matrix Degradation in Breast Cancer Tumors Improves Therapy by Trastuzumab

2011 ◽  
Vol 19 (3) ◽  
pp. 479-489 ◽  
Author(s):  
Ines Beyer ◽  
Zongyi Li ◽  
Jonas Persson ◽  
Ying Liu ◽  
Ruan van Rensburg ◽  
...  
2009 ◽  
Vol 69 (3) ◽  
pp. 747-752 ◽  
Author(s):  
Inmaculada Ayala ◽  
Giada Giacchetti ◽  
Giusi Caldieri ◽  
Francesca Attanasio ◽  
Stefania Mariggiò ◽  
...  

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Maren Hülsemann ◽  
Colline Sanchez ◽  
Polina V. Verkhusha ◽  
Vera Des Marais ◽  
Serena P. H. Mao ◽  
...  

AbstractDuring breast cancer metastasis, cancer cell invasion is driven by actin-rich protrusions called invadopodia, which mediate the extracellular matrix degradation required for the success of the invasive cascade. In this study, we demonstrate that TC10, a member of a Cdc42 subfamily of p21 small GTPases, regulates the membrane type 1 matrix metalloproteinase (MT1-MMP)-driven extracellular matrix degradation at invadopodia. We show that TC10 is required for the plasma membrane surface exposure of MT1-MMP at these structures. By utilizing our Förster resonance energy transfer (FRET) biosensor, we demonstrate the p190RhoGAP-dependent regulation of spatiotemporal TC10 activity at invadopodia. We identified a pathway that regulates invadopodia-associated TC10 activity and function through the activation of p190RhoGAP and the downstream interacting effector Exo70. Our findings reveal the role of a previously unknown regulator of vesicular fusion at invadopodia, TC10 GTPase, in breast cancer invasion and metastasis.


2020 ◽  
Author(s):  
M. Hülsemann ◽  
S.K. Donnelly ◽  
P.V. Verkhusha ◽  
S.P.H. Mao ◽  
J.E. Segall ◽  
...  

AbstractDuring breast cancer metastasis, cancer cell invasion is driven by actin-rich protrusions called invadopodia, which mediate the extracellular matrix degradation required for the success of the invasive cascade. In this study, we demonstrated that TC10, a member of a Cdc42 subfamily of p21 small GTPases, regulates the membrane type 1 matrix metalloproteinase (MT1-MMP)-driven extracellular matrix degradation at invadopodia. We show that TC10 is required for the plasma membrane surface exposure of MT1-MMP at invadopodia. By utilizing our new Förster resonance energy transfer (FRET) biosensor, we demonstrated the p190RhoGAP-dependent regulation of spatiotemporal TC10 activity at invadopodia. We identified a pathway that regulates TC10 activity and function at invadopodia through the activation of p190RhoGAP and the downstream interacting effector Exo70 at the invadopodia sites. Our findings reveal the role of a previously unknown regulator of vesicular fusion at invadopodia, TC10, on the invasive potential of breast cancer cells during invasion and metastasis.


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