Fig. 1
From: Targeting oral tumor microenvironment for effective therapy
The interactions of CAFs with OSCC. CAFs have positive cross-talk with OSCC cells. Deposition of collagen and also the release of lactate acid prevent penetration of CD8 + T cells into the tumor and exhaust the activity of infiltrated CD8 + T cells. OSCC cells trigger the release of IL-33 by CAFs, leading to the inhibition of apoptosis signaling pathways in OSCC cells. The release of some other cytokines may cause overexpression of VEGF and the induction of angiogenesis. Furthermore, overexpression of HAS2 in CAFs and stimulation of the Wnt/β-catenin in OSCC cells facilitate invasion and metastasis. (CAF: Cancer-associated fibroblast; DR: Dead receptor; EGF: Epidermal growth factor; EGFR: Epidermal growth factor receptor; EMT: epithelial-mesenchymal transition; HAS2: Hyaluronan synthetase 2; TGF-β: transforming growth factor-β; MMP: Matrix metalloproteinase; NF-κB: nuclear factor-κB; PI3K: Phosphoinositide 3-kinase; SDF-1: Stromal cell-derived factor-1; STAT: Signal transducer and activator of transcription; VEGF: Vascular endothelial growth factor)