Skip to main content
. Author manuscript; available in PMC: 2025 Aug 27.
Published in final edited form as: Semin Liver Dis. 2025 Mar 5;45(1):33–51. doi: 10.1055/a-2551-0724

Figure 3. Functions and mediators of aHSC in HCC and HSC-derived CAF in iCCA.

Figure 3.

aHSC in HCC and HSC-derived CAFs in iCCA produce a wide range of mediators that can modulate critical pathways affecting tumor growth, neoangiogenesis and immunosuppression, within others. Depending on the context, those mediators can be tumor promoting, tumor restrictive or have no effects on the PME nor the TME. Here are shown few of these mediators.

ANGPT1/2, Angiopoietin; CCL2, C-C motif chemokine ligand 2; CCR2, C-C motif chemokine receptor 2; CD44, Cluster of differentiation 44; COL1A1, Collagen type 1 alpha 1 chain; COX-2, Cyclooxygenase-2; CXCL12, C-X-C motif chemokine ligand 12; DDR-1, Discoidin domain receptor 1; EGF, Epidermal growth factor; Fas, Fas cell surface death receptor; FasL, Fas ligand; FGF, Fibroblast growth factor; HAS2, Hyaluronan synthase 2; HGF, Hepatocyte growth factor; IL-10, Interleukin 10; IL-6, Interleukin 6; MDSC, Myeloid-derived suppressor cell; MET, MET proto-oncogene receptor tyrosine kinase; PDGF, Platelet derived growth factor; POSTN, Periostin; Spp1, Secreted phosphoprotein 1; TAM, Tumor associated macrophage; TGF-β, Transforming growth factor beta; TNC, Tenascin, Treg, regulatory T cells; VEGF, Vascular endothelial growth factor.