scholarly journals Fluid shear stress stimulates breast cancer cells to display invasive and chemoresistant phenotypes while upregulating PLAU in a 3D bioreactor

2019 ◽  
Vol 116 (11) ◽  
pp. 3084-3097 ◽  
Author(s):  
Caymen M. Novak ◽  
Eric N. Horst ◽  
Charles C. Taylor ◽  
Catherine Z. Liu ◽  
Geeta Mehta
Keyword(s):  
Breast Cancer ◽  
Shear Stress ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Fluid Shear Stress ◽  
Fluid Shear

scholarly journals Cellular Mechanisms of Circulating Tumor Cells During Breast Cancer Metastasis

2020 ◽  
Vol 21 (14) ◽  
pp. 5040 ◽  
Author(s):  
Han-A Park ◽  
Spenser R. Brown ◽  
Yonghyun Kim
Keyword(s):  
Breast Cancer ◽  
Shear Stress ◽  
Oxidative Phosphorylation ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cancer Metastasis ◽  
Fluid Shear Stress ◽  
Breast Cancer Metastasis ◽  
Fluid Shear ◽  
Cellular Mechanisms

Circulating tumor cells (CTCs) are cancer cells that detach from the primary site and travel in the blood stream. A higher number of CTCs increases the risk of breast cancer metastasis, and it is inversely associated with the survival rates of patients with breast cancer. Although the numbers of CTCs are generally low and the majority of CTCs die in circulation, the survival of a few CTCs can seed the development of a tumor at a secondary location. An increasing number of studies demonstrate that CTCs undergo modification in response to the dynamic biophysical environment in the blood due in part to fluid shear stress. Fluid shear stress generates reactive oxygen species (ROS), triggers redox-sensitive cell signaling, and alters the function of intracellular organelles. In particular, the mitochondrion is an important target organelle in determining the metastatic phenotype of CTCs. In healthy cells, mitochondria produce adenosine triphosphate (ATP) via oxidative phosphorylation in the electron transport chain, and during oxidative phosphorylation, they produce physiological levels of ROS. Mitochondria also govern death mechanisms such as apoptosis and mitochondrial permeability transition pore opening to, in order eliminate unwanted or damaged cells. However, in cancer cells, mitochondria are dysregulated, causing aberrant energy metabolism, redox homeostasis, and cell death pathways that may favor cancer invasiveness. In this review, we discuss the influence of fluid shear stress on CTCs with an emphasis on breast cancer pathology, then discuss alterations of cellular mechanisms that may increase the metastatic potentials of CTCs.

scholarly journals Upregulation of COX-2 in MCF7 Breast Cancer Cells When Exposed to Shear Stress

OBM Genetics ◽  
2019 ◽  
Vol 3 (3) ◽  
pp. 1-1
Author(s):  
Caymen M. Novak ◽  
◽  
Eric N. Horst ◽  
Shreya Raghavan ◽  
Geeta Mehta ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Shear Stress ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cox 2

scholarly journals Cancer cells resist mechanical destruction in the circulation via RhoA-myosin II axis

2019 ◽  
Author(s):  
Devon L. Moose ◽  
Benjamin L. Krog ◽  
Lei Zhao ◽  
Tae-Hyung Kim ◽  
Sophia Williams-Perez ◽  
...  
Keyword(s):  
Shear Stress ◽  
Cancer Cells ◽  
Mouse Models ◽  
Fluid Shear Stress ◽  
Myosin Ii ◽  
Membrane Damage ◽  
Fluid Shear ◽  
Mechanical Destruction ◽  
Primary Tumors ◽  
Hemodynamic Forces

ABSTRACTDuring metastasis cancer cells are exposed to potentially destructive hemodynamic forces including fluid shear stress (FSS) whileen routeto distant sites. However, prior work indicates that cancer cells are more resistant to brief pulses of high-level fluid shear stress (FSS)in vitrorelative to non-transformed epithelial cells. Herein we identify a mechanism of FSS resistance in cancer cells, and extend these findings to mouse models of circulating tumor cells (CTCs). We show that cancer cells acutely isolated from primary tumors are resistant to FSS. Our findings demonstrate that cancer cells activate the RhoA-myosin II axis in response to FSS, which protects them from FSS-induced plasma membrane damage. Moreover, we show that the myosin II activity is protective to CTCs in mouse models. Collectively our data indicate that viable CTCs actively resist destruction by hemodynamic forces and are likely to be more mechanically robust than is commonly thought.

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