Skip to main content

Table 3 The effects and mechanisms of CAFs on HCC cells/CCA cells

From: Advances of cancer-associated fibroblasts in liver cancer

  HCC-CAFs CCA-CAFs
Mediator Effects and mechanisms in HCC Mediator Effects and mechanisms in CCA
chemoresistance HGF CAF-derived HGF enhances the resistance of HCC cells to sorafenib and cisplatin by upregulating the expression of CD73 [18] PIGF Antagonizing CAF-secreted PIGF can alleviate chemoresistance effects [141]
CAFs-supernatants CAF supernatant induces RCN1 expression in HCC cells, thereby enhancing resistance to sorafenib via the IRE1α-XBP1s pathway [48] IGF2 CAFs-secreted IGF2 stimulated IR/IGF1R signaling activation in erlotinib-resistant CCA cells [143]
IL6 CAF-secreted IL6 attenuates the sensitivity of CCA cells to chemotherapeutic drugs by inhibiting autophagy in CCA cells [146]
Cancer stemness IL6 CAFs-secreted HGF and IL6 enhanced stemness of CD24 + HCC cells through activated STAT3 pathway [57] IL6 CD146-positive vascular CAFs (vCAFs)-secreted IL6 enhanced the stemness of CCA [47]
HGF CAFs-derived HGF enhanced stemness via (ERK)1/2–FRA1–HEY1 pathway [51] MDSCs CAFs indirectly regulated tumor stemness by recruiting MDSCs in the TME of CCA [90]
HGF induces KRT19 expression in HCC cells via the MET-ERK1/2-AP1 and SP1 axis, thereby promoting stemness maintenance [54]
FSTL1 CAFs-derived FSTL1 promoted the stemness through the AKT/mTOR/4EBP1 signaling pathways [60]
CLCF1 CAF-secreted CLCF1 enhances stemness by promoting the secretion of CXCL6 and TGF in HCC cells [61]
FOXQ1 CAF promotes HCC initiation via the FOXQ1/NDRG1 axis [63]
RvD1 RvD1 inhibits CAF-secreted COMP to antagonize the stemness effect via FPR2/ROS/FOXM1 signaling [69]
angiogenesis VEGF CAFs-derived VEGF promote the angiogenesis via EZH2 /VASH1 pathway [94] VEGF VEGF secreted by CAFs promoted the chemotaxis and assembly of lymphatic endothelial cells [161]
PIGF CD90 positive CAFs have a strong correlation with PIGF expression in HCC tissues [96] PIGF PIGF produced by CAFs could compress the tumor vessel and deteriorate the hypoxic state in CCA [141]
TGF-β and SDF1 CAFs-derived TGF-β and SDF1 facilitated VM formation [97]
prolargin CAFs-secreted prolargin inhibited the angiogenesis of HCC [45]
SPARCL1 SPARCL1-positive fibroblasts could maintain the self-stabilization of blood vessels [41]