Intersecting pathways in inflammation and cancer: Hepatocellular carcinoma as a paradigm

Figure 1 The intrinsic and extrinsic pathways combine to create a local microenvironment around the injured and transformed hepatocyte to augment tumor promoting mechanisms. ROS: Reactive oxygen species; HIF1α: Hypoxia inducible factor 1 alpha; NK cell: Natural killer cell; MDSC: Myeloid derived suppressor cell; IL: Interleukin; TGF-β: Transforming growth factor Beta; HGF: Hepatocyte growth factor; NF-κB: Nuclear factor kappa-light-chain-enhancer of activated B cells; CXCL: Chemokine ligand; STAT3: Signal transducer and activator of transcription 3.

Figure 2 The complex cellular network in the tumor microenvironment mediated by chemokines, cytokines, and cellular transcription factors. NK cell: Natural killer cell; MDSC: Myeloid derived suppressor cell; IL: Interleukin; TGF- β:Transforming growth factor Beta; αSMA: Alpha smooth actin; FSP-1: Fibroblast specific protein; PDGF: Platelet derived growth factor; Hh: Hedgehog; NF-κB: Nuclear factor kappa-light-chain-enhancer of activated B cells; CXCL: Chemokine ligand; STAT3: Signal transducer and activator of transcription 3; Treg: T regulatory cells; MT-MMP: Membrane type matrix metalloproteinase; HNF-4: Hepatocyte nuclear factor-4; EMT: Epithelial-mesenchymal-transition; MIF: migration inhibitory factor.