miR-27b-3p directly targets PPARG to regulate pancreatic cancer progression

miR-27b-3p is dysregulated in many cancers, but its expression, clinical role, and mechanism in pancreatic cancer are not fully understood. This study aimed to evaluate the clinical value of miR-27b-3p in PC and its role in pancreatic cancer (PC) progression by targeting PPARG. qRT-PCR was used to measure miR-27b-3p and PPARG levels in 106 paired PC tissues and adjacent non-tumor tissues, and in PC cell lines (PANC-1, SW1990, BxPC-3, AsPC-1) and HPDE cells. Kaplan-Meier and multivariate Cox analyses assessed miR-27b-3p prognostic value. CCK-8 and Transwell assays evaluated the impact of miR-27b-3p inhibition on PC cell function. Dual-luciferase reporter and Pearson correlation analyses confirmed the targeting of PPARG by miR-27b-3p. A PPARG knockdown rescue experiment verified that miR-27b-3p function depends on PPARG. miR-27b-3p was highly expressed in PC tissues and cell lines and linked to lymph node metastasis, distant metastasis, elevated CA19-9 levels, and poor overall survival. Multivariate Cox analysis showed high miR-27b-3p expression as an independent predictor of poor prognosis. In vitro, miR-27b-3p inhibition suppressed PANC-1 cell proliferation, migration, and invasion. PPARG was a direct target of miR-27b-3p and was downregulated at both mRNA and protein levels. A negative correlation was found between miR-27b-3p and PPARG mRNA in PC tissues. PPARG knockdown reversed the effects of miR-27b-3p inhibition, confirming functional dependence. miR-27b-3p functions as an oncogenic miRNA in PC by targeting PPARG and may be a prognostic biomarker and therapeutic target.