Inhibition of fatty acid binding protein suppresses pancreatic cancer progression and metastasis.

ABSTRACT: Obesity is a known risk factor for Pancreatic ductal adenocarcinoma (PDAC). Fatty acid binding protein 4 (FABP4) is higher in plasma of obese patients, and linked to the progression of obesity-related cancers. To provide insights into the role of FABP4 in PDAC progression and determine the potential of FABP4 inhibitor for PDAC treatment, we elucidated the anticancer mechanism of FABP4 inhibition using FABP4 null mice and FABP4 inhibitor (HTS01037). In vitro, HTS010137 suppressed FABP4-induced cell viability in mouse (KPC cells) and human PDAC cell lines. FABP4 promoted invasive potency, epithelial-mesenchymal transition (EMT), and cancer stemness markers that were associated with up-regulation of transcription factor ZEB1. In vivo, both FABP4 knockout and inhibition with HTS01037 suppresse

SUBMITTER: Shinoda S 

PROVIDER: S-EPMC12274511 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature