Table 3.
Subtypes and comparisons of CAFs.
| Subtype | Main gene | Function | Clinical significance |
|---|---|---|---|
| myCAF | ACTA2 (α-SMA), TAGLN, MYL9, CNN | High contractility, generating a large amount of ECM; It forms a physical barrier that hinders T cell infiltration and drug delivery; It is usually strongly activated by the TGF-β signaling pathway |
It may be related to tumor hardness, invasion, metastasis and immune rejection |
| iCAF | IL6, LIF, CXCL12, CXCL1, CXCL2, | Secrete a large amount of cytokines and chemokines; Recruit myeloid cells and induce immunosuppression; Promote the stemness and survival of tumor cells; It is usually driven by the IL-1α/β and NF-κB signaling pathways. |
It may be related to immunosuppression, inflammation and resistance to chemotherapy. |
| apCAF | CD74, MHC-II | It expresses MHC-II class molecules but lacks co-stimulatory molecule; It may mediate the impotence or inhibition of CD4+ T cells rather than their activation. |
Unclear |
| meCAF | CAV1, ALDH1A | Metabolic reprogramming to support the metabolic needs of tumors; Nourish tumor cells through nutrients |
It may be related to tumor growth, metabolic adaptation and treatment resistance. |