Project description:The hypoxic tumor microenvironment is a critical driver of pancreatic ductal adenocarcinoma (PDAC) progression and chemoresistance. However, a comprehensive, multi-omics resource systematically profiling the molecular alterations induced by chronic hypoxia across diverse cellular components of PDAC is currently lacking. Here, we present a deeply characterized dataset generated from three PDAC cell lines, one pancreatic stellate cell line, and one normal pancreatic ductal epithelial cell line cultured under normoxic and chronic hypoxic (1% O₂) conditions. The dataset includes matched transcriptomic (RNA-Seq), proteomic, and phosphoproteomic profiles from biologically triplicated samples, all supported by phenotypic validation data confirming hypoxia-induced proliferation and gemcitabine resistance.
Project description:The goal of this study was to determine IGF2BP3 regulation of RNA targets in human pacreatic ductal adenocarcinoma cell lines Included are iCLIP-seq libraries for IGF2BP3 from PL45 and Panc1 PDAC cell samples, RIP-seq samples from PL45 and Panc1 PDAC cells, RNA-seq data sets from control and IGF2BP3 knockdown in PL45 and Panc1 PDAC cells, and small RNA-seq samples from Panc1 cells
Project description:This study aimed to analyze ductal and squamous marker expression in pancreatic ductal adenocarcinoma (PDAC) cell lines under two-dimensional (2D) and three-dimensional (3D) culture conditions. Eight PDAC cell lines were examined using nanoLC-MS/MS-based proteomics.
Project description:We demonstrate that a clinically relevant X-ray hypofractionation regimen (3x8 Gy) of multiple PDAC cel lines effectively induces immunogenic cell death and transactivates Interferon beta-1 in a STING-dependent manner. RNA-seq analyses showed a global and steady upregulation of type I interferon response in PDAC cells following 3x8 Gy.