Fig. 6: CAFs divide into myofibroblastic CAFs (myCAFs) and proteolytic inflammatory CAFs (piCAFs) in human CRC.
From: Fibroblast dynamics in colorectal cancer: stability, plasticity, and novel markers
a CTHRC1 and FAP are evenly expressed by all CAFs. b CAFs divide into myofibroblastic CAFs (myCAF) and proteolytic inflammatory CAFs (piCAFs). c ACTA2 and TAGLN separate myCAFs from MMP1 and MMP3 expressing piCAFs. d Heat map of the top-ranking subpopulation specific genes of myCAFs and piCAFs. PiCAFs are characterized by elevated MMP1, MMP3, CXCL8 and IL6 expression. MyCAFs express ACTA2, TAGLN and MYL9. e Spearman correlation of mRNA expression of individual genes representative for the piCAF subpopulation with myCAF markers in the COAD tumor and READ tumor cohort. f Isolated CAFs in vitro preserve the myCAF phenotype, whereas piCAFs are depleted. g Pathway analysis of the most significantly upregulated MSigDB_Hallmark_2020 terms of myCAFs and piCAFs. h High expression of myCAF markers (ACTA2, TAGLN, MYL9) is associated with worse prognosis for CRC patients (OS: p = 0.00093, RFS: p = 3.1e−12), whereas expression of the piCAF subpopulation markers (MMP1, MMP3, CXCL8) does not correlate with survival (OS: p = 0.65, RFS: p = 0.8). High expression was defined using the upper tertile of the total cohort.
