Table 1 Phenotype and heterogeneity of CAF
From: Signaling pathways in cancer-associated fibroblasts and targeted therapy for cancer
Tissue type | Phenotype | Markers | Origin and/or function | Ref. |
|---|---|---|---|---|
BC (human) | CAF-S1 | CD29Med, FAPHi, FSP1Med, α-SMAHi, PDGFRβMed-Hi, CAV-1Low | Regulatory of cancer invasion and immune response | |
CAF-S2 | CD29Low, FAPNeg, FSP1Neg-Low, α-SMANeg, PDGFRβNeg, CAV-1Neg | ND | ||
CAF-S3 | CD29Med, FAPNeg, FSP1Med-Hi, α-SMANeg-Low, PDGFRβMed, CAV-1Neg-Low | ND | ||
CAF-S4 | CD29Hi, FAPNeg, FSP1Low-Med, α-SMAHi, PDGFRβLow-Med, CAV-1Low | Regulatory of actin cytoskeleton and oxidative metabolism | ||
OSCC (human) | CAF-N | KGF | High fibroblast motility | |
CAF-D | TGF-β1 | Low fibroblast motility | ||
NF | HGF, MMP3 | Lower tumor incidence | ||
LC (human) | Cluster 1 | COL10A1 | Showing a strong EMT signals | |
Cluster 2 | COX4I2, ACTA2, MEF2C | Regulatory of myogenesis and angiogenesis | ||
Cluster 3 | ND | Upregulating collagen and ECM molecules expression | ||
Cluster 4 | PLA2G2A | Similar to cluster 1 | ||
Cluster 5 | MMP3 | Low myogenesis and high mTOR expression | ||
Cluster 6 | FIGF | Representing nonmalignant fibroblasts | ||
Cluster 7 | ND | Similar to cluster 4 but differing in the glycolysis pathway | ||
CRC (human) | CAF-A | MMP2, DCN, COL1A2 | Regulatory of ECM remodeling and express FAP | |
CAF-B | ACTA2, PDGFA, TAGLN | Activation of cytoskeletal gene | ||
NF | MGP (ND) | ND | ||
HNSCC (human) | CAF1 | CTHRC1, COL1A1, POSTN, TPM4, MFAP2 (ND) | Promoting cancer metastasis | |
CAF2 | CFD, APOD, CXCL12, GPC3, SEPP1 (ND) | |||
NF | Depleted of markers for myofibroblasts and CAFs | Resting fibroblasts | ||
OC (human) | FAP-high CAF | FAP, TGF-β, COL11A1, SULF1, IL-6, CXCL12 | Regulatory of cancer invasion and immune regulation | |
FAP-low CAF | DLK1, TCF21, COLEC11 | Regulatory of glucose homeostasis, lipid metabolism, etc. | ||
NF | COMP, SFRP2, GJB2 (ND) | ND | ||
BC (mouse) | mCAF | Fibulin-1, PDGFRα | From resident fibroblast/regulatory of tumor immune response | |
vCAF | Nidogen-2 | From vasculature/promoting vascular development | ||
cCAF | Ki-67 | Representing the proliferative segment of vCAF | ||
dCAF | SCRG1 | From malignant cell/locating on tumor–stroma boundary | ||
PDAC (mouse) | myCAF | α-SMA | Adjacent to tumor cells and promoting desmoplasia | |
iCAF | IL-6, LIF | Locating away within stroma and promotes tumor progression | ||
NF | ND | Pancreatic stellate cells | ||
BC (mouse) | Cluster 0 | Ly6c1 | From resident fibroblasts/promoting cancer progression and immune evasion | |
Cluster 1 | α-SMA | Promoting cancer development and progression | ||
Cluster 2 | Cdk1 | Identifying as dividing cells | ||
Cluster 3 | Cd53 | High transcriptional enrichment for desmin | ||
Cluster 4 | Crabp1 | From Ly6c1high fibroblasts | ||
Cluster 5 | Cd74 | Expressing MHC class II and regulatory of immune-modulatory | ||
HCC (ND) | Activated myofibroblast phenotype | α-SMA, FAP, vimentin, vollagen 1α, PDGFRα, FN | Maintaining and enhancing the stemness of HCC cells | |
Mesenchymal stromal cell phenotype | CD90, CD73, CD105, CD29, CD44, CD166 | Regulatory of immunosuppression |
