Publication date: 25th July 2016
Metastasis, the process by which cancer cells travel from a primary tumor to establish lesions in distant organs, is the cause of most cancer-related deaths. One critical process during metastasis is the transit of cells from a primary tumor and through the vasculature or lymphatic systems to a distant site. However, visualization of cellular behavior in the vasculature is difficult in most model systems, where final cell destination is not known beforehand. Here, we used subclones of breast adenocarcinoma cells injected into the circulation of embryonic zebrafish as a model xenograft system of metastasis. The zebrafish vasculature contains vessels on the scale of human capillaries. Real-time intravital imaging revealed metastatic spread to be an inefficient process, with less than 20% of cells passing through a given organ remaining there following 14 h of imaging. Additionally, there was no significant difference in the organ-specific residence time or migration speed of cells of each clone in the organ vasculature. Instead, cell capture and migration rate were dependent on vessel topography, and groups of cells had both longer residence times and greater interactions with host macrophages and neutrophils. To elucidate the role of topography in the absence of host cells, we engineered a microfluidic device containing microchannels with cross-sectional area on the scale of the vasculature. Again, cell migration speed was not dependent on ECM but was instead dictated by topography. Our findings indicate that local topography and not ECM composition drives early metastatic spread.
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