Anti-fibrotic effect of isorhamnetin and its derivatives on disruption of pancreatic ductal adenocarcinoma desmoplasia by regulation of cancer-associated fibroblasts

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Taken together, our findings demonstrated that isorhamnetin impaired human PDAC CAFs mitochondrial respiration and glycolysis with mitochondrial loss and caused cell death and cell cycle arrest. In particular, iCAF markers were strongly inhibited which might drive CAFs to shift from inflammatory to myofibroblast-like phenotype as observed by the moderate increase in ACTA2 gene expression although other myCAFs markers were reduced, suggesting general benefic effects of isorhamnetin which could contribute for further investigation of PDAC therapy targeting CAFs metabolism and crosslink between CAFs and tumor cells.