Overview of tumor-immune crosstalk inside the tumor microenvironment identified using microfluidic technology at the bulk-cell level in this review. (IMAGE)

China Anti-Cancer Association

Overview of tumor-immune crosstalk inside the tumor microenvironment identified using microfluidic technology at the bulk-cell level in this review.

Caption

Overview of tumor-immune crosstalk inside the tumor microenvironment identified using microfluidic technology at the bulk-cell level in this review. (A) IL-8, CCL2, and CSF-1 derived from cancer cells enhance macrophage migration. M2a macrophages promote cancer aggregate dispersal when in contact with the cancer aggregates. NETs formed in the extracellular collagen matrix predominantly mediate collective tumor invasion. TNF-α secreted by macrophages increases endothelial permeability and regulates cancer cell intravasation. ECM, extracellular matrix; IL-8, interleukin 8; CCL2, C-C motif chemokine ligand 2; CSF-1, colony stimulating factor-1; TNF-α, tumor necrosis factor alpha; NETs, neutrophil extracellular traps. (B) Monocytes could increase T-cell infiltration into tumor loci, while stromal cells form a physical barrier that protects cancer cells from immune cell infiltration and recognition. (C) Inflamed neutrophils interact with cancer cells in blood vessels and secrete IL-8 to disrupt the endothelial barrier and promote cancer cell extravasation. Macrophages remold ECM and generate micro-tracks to allow extravasated cancer cells to sustain high invasiveness. (D) Monocytes can directly reduce cancer cell extravasation in a non-contact dependent manner in blood vessels. (E) Trastuzumab prolongs the interaction time between cancer cells and PBMC and induces an ADCC immune response, while CAFs antagonize this effect. PBMC, peripheral blood mononuclear cell; ADCC, antibody-dependent cell-mediated cytotoxicity; CAF, cancer-associated fibroblast. (F) In vivo-like CSF flow is recreated using dynamic fluid flow and applied to the microfluidic platform to recapitulate the choroid plexus dynamic microenvironment. HER2 expression on cancer cells is significantly higher in the dynamic condition compared to the static condition. Macrophages enhance the cytotoxic effects of anti-HER2 therapy. CSF, cerebrospinal fluid; HER2, human epidermal growth factor receptor 2.

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Cancer Biology & Medicine

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