Pancreatic　ductal　adenocarcinoma　(PDAC)　is　a　devastating　cancer　with　a　dismal　prognosis　due　to　distant　metastasis.　Through　an　analysis　of　large　RNA　sequencing　and　proteomics　datasets,　we　found　that　high　KRT7　expression　in　PDAC　patients　was　correlated　with　liver　metastasis　and　poor　survival.　A　functional　investigation　revealed　that　the　overexpression　of　KRT7　promoted　liver　metastasis　but　did　not　affect　tumor　cell　proliferation　in　vivo　or　in　vitro.　Analysis　of　scRNA-Seq　data　from　24　PDAC　samples　revealed　a　negative　correlation　between　KRT7　expression　in　PDAC　cells　and　cancer-associated　fibroblast　(CAF)　infiltration,　and　this　was　further　confirmed　in　orthotopic　tumor　model　mice　injected　with　KRT7-overexpressing　PDAC　cells,　which　led　the　development　of　to　a　prometastatic　niche　with　reduced　ECM　deposition.　Mechanistically,　KRT7　in　PDAC　cells　promoted　the　secretion　of　FGF2,　which　inhibited　CAF　proliferation　and　ECM-related　gene　transcription　through　the　Wnt/beta-catenin　pathway.　Moreover,　targeting　FGF2　decreased　liver　metastasis　in　vivo.　Our　study　revealed　that　KRT7　promotes　PDAC　liver　metastasis　by　remodeling　the　extracellular　matrix　niche　through　FGF2-fibroblast　crosstalk　and　provides　a　promising　strategy　for　preventing　PDAC　liver　metastasis.