FABP4 interacts with PPARγ to promote malignant progression in pancreatic cancer

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Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with an exceptionally poor prognosis. Fatty acid-binding protein 4 (FABP4) has been implicated in tumorigenesis and peroxisome proliferator-activated receptor γ (PPARγ) signaling, but its precise functional role and underlying molecular mechanisms in PDAC remain poorly defined. Here, we showed that FABP4 is markedly upregulated in pancreatic cancer cells. Co-immunoprecipitation assays revealed an interaction between FABP4 and PPARγ, and FABP4 overexpression significantly enhanced pancreatic cancer cell viability, proliferation, and migratory capacity in vitro . Moreover, FABP4 overexpression was associated with increased lipid metabolic activity and reduced sensitivity to ferroptosis, and it substantially promoted the tumorigenic potential of PANC-1 cells in vivo . Notably, pharmacological inhibition of PPARγ effectively attenuated the malignant phenotypes elicited by FABP4 overexpression in pancreatic cancer cells, underscoring that PPARγ is critically involved in the FABP4-associated tumor progression phenotype.

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