FABP4 overexpression enhanced pancreatic cancer cell viability, proliferation, and in vivo tumorigenic potential, which was effectively attenuated by pharmacological inhibition of PPARγ.
Does FABP4 interact with PPARγ to promote malignant progression in pancreatic cancer?
FABP4 interacts with PPARγ to promote malignant progression in pancreatic cancer, suggesting a potential therapeutic target.
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.
Yang et al. (2026) studied Pancreatic ductal adenocarcinoma. FABP4 overexpression and PPARγ inhibition was evaluated on Cell viability, proliferation, migratory capacity, and tumorigenic potential. FABP4 overexpression enhanced pancreatic cancer cell viability, proliferation, and in vivo tumorigenic potential, which was effectively attenuated by pharmacological inhibition of PPARγ.