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Vascular adhesion of circulating tumor cells (CTCs) is a key step in cancerspreading. If inflammation is recognized to favor the formation of vascularmetastatic niches, little is known about the contribution of blood rheology toCTC deposition. Herein, a microfluidic chip, covered by a confluent monolayerof endothelial cells, is used for analyzing the adhesion and rolling ofcolorectal (HCT 15) and breast (MDA MB 231) cancer cells under differentbiophysical conditions. These include the analysis of cell transport in aphysiological solution and whole blood; over a healthy and a TNF alpha inflamedendothelium; with a flow rate of 50 and 100 nL/min. Upon stimulation of theendothelial monolayer with TNF alpha (25 ng/mL), CTC adhesion increases by 2 to4 times whilst cell rolling velocity only slightly reduces. Notably, wholeblood also enhances cancer cell deposition by 2 to 3 times, but only on theunstimulated vasculature. For all tested conditions, no statisticallysignificant difference is observed between the two cancer cell types. Finally,a computational model for CTC transport demonstrates that a rigid cellapproximation reasonably predicts rolling velocities while cell deformabilityis needed to model adhesion. These results would suggest that, withinmicrovascular networks, blood rheology and inflammation contribute similarly toCTC deposition thereby facilitating the formation of metastatic niches alongthe entire network, including the healthy endothelium. In microfluidic basedassays, neglecting blood rheology would significantly underestimate themetastatic potential of cancer cells.

Deciphering the relative contribution of vascular inflammation and blood rheology in metastatic spreading