![]() Collectively, our study reveals that IF could be a critical regulator of tumor immune environment.Ĭancer is a complex disease that depends not only on cancer cells themselves but also on the environment in which they reside. Since IF emanates from the tumor to the surrounding stromal tissues, our results suggest that IF could not only induce M2 polarization of macrophages but also recruit these M2 macrophages toward the tumor masses, contributing to cancer cell invasion and tumor progression. Moreover, IF directs macrophages to migrate against the flow. Consistent with this flow-induced M2 polarization, macrophages treated with IF migrate faster and have an enhanced ability to promote cancer cell migration. Specifically, interstitial flow (IF) polarizes macrophages toward an M2-like phenotype via integrin/Src-mediated mechanotransduction pathways involving STAT3/6. Here, we used three-dimensional biomimetic models to reveal that macrophages can sense and respond to pathophysiological levels of interstitial fluid flow reported in tumors (∼3 µm/s). ![]() While it is well established that chemical stimuli within the tumor tissues can alter macrophage behaviors, the effects of mechanical stimuli, especially the flow of interstitial fluid in the tumor microenvironment, on macrophage phenotypes have not been explored. Macrophages in the tumor microenvironment are key contributors to tumor progression. Tumor tissues are characterized by an elevated interstitial fluid flow from the tumor to the surrounding stroma.
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