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. 2020 Dec 9;10:602661. doi: 10.3389/fonc.2020.602661

Figure 2.

Figure 2

The oral squamous cell carcinoma (OSCC) tumor microenvironment. (A) The OSCC tumor microenvironment is mainly composed of cancer-associated fibroblasts (CAFs). CAFs derive from normal fibroblasts after autocrine stimulation of chemokine (C-X-C motif) ligand (CXCL1) chemokine through a nuclear factor κB (NFκB)-dependent mechanism. NFκB is activated in fibroblasts by the action of interleukin-1β (IL1β) released from OSCC cells. Conditions surrounding the tumoral tissue, such as increased levels of platelet-derived growth factor (PDGF) and IL1β or hypoxia activate Janus kinase (JAK)/STAT and NFκB pathways in CAFs, which induce the release of chemokines (CCL2 and CCL7) and epithelial growth factor (EGF), or inhibit the release of selective miRs such as miR-34a-5p. All these mediators augment proliferation and EMT of OSCC cells. (B) CAFs release well known anti-inflammatory molecules such as IL10 and TGFβ that attract anti-inflammatory macrophages and regulatory T-cells, T-regs, and inhibit proliferation of T-cells.