Fig. 2

Tumor microenvironment (TME) and radioresistance. (A) CAF induces monocyte MDSC production through STAT3 signaling activated by IL-6/exosomal miR-21. (B) CAF crosstalk with TAM through the inflammatory CXCL12-CXCR4 axis. (C) CAF provides cancer cells with amino acids, fatty acids, glucose, phospholipids and glycerides that are essential for ESCC growth; and enhances escape through E-cadherin/N cadherin linkage enhances escape. (D) Cancer cells secrete hydrogen peroxide, which increases oxidative stress in CAF and induces a shift in the metabolic environment of CAF from oxidative phosphorylation to aerobic glycosylation, further providing cancer cells with lactate and pyruvate. (E) CAF secretions, including pro-tumor factors, proteins, inflammatory factors, growth factors, and non-coding RNAs induce migration and invasion of ESCC cells. (F) TAM provides ESCC cells with a variety of amino acids through AKT/mTOR, AKT/ERK and AKT/p38 MAPK induce ESCC cell growth, migration and invasion. (G,H) Regulatory T cell (Treg) mediate ESCC evasion of immune responses through expression of the immunosuppressive factor COX-2, whose interaction with TAM via ligand-receptor interactions may contribute to the immunosuppressed state and disease progression