Fig. 4.

Schematic diagram of the interaction of CAF with cells in BC and PDAC TME. The IL6-adenosine loop potentiates immunosuppression and BC progression, and the TIMP-1/CD63/integrin β1/STAT3 loop is associated with BC cell growth. Erdafitinib promotes T lymphocyte infiltration via inhibiting MARK/ERK signaling. Moreover, CAF-secreted TGF-β1 activates the transcription of HOTAIR to promote BC cell metastasis; the autocrine TGF-β1/miR-200 s/miR-221/DNMT3B loop maintains CAF activity and promotes BC progression. CAF-secreted CXCL12 favors BC cell proliferation and EPC, LAM recruitment. In PDAC, CAF reduction can be achieved by depleting or reprogramming CAF. CAF-derived circFARP1 and TGF-β can both lead to gemcitabine resistance in PDAC cells, and CAF-secreted Hh promotes EMT via upregulating SNAIL transcription. In the end, Hh inhibition changes the proportion of CAF phenotypes in PDAC TME. By Biorender