Temporally resolved proteomics identifies nidogen-2 as a cotarget in pancreatic cancer that modulates fibrosis and therapy response.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is characterized by increasing fibrosis, which can enhance tumor progression and spread. Here, we undertook an unbiased temporal assessment of the matrisome of the highly metastatic KPC (Pdx1-Cre, LSL-Kras^G12D/+, LSL-Trp53^R172H/+) and poorly metastatic KP^flC (Pdx1-Cre, LSL-Kras^G12D/+, Trp53^fl/+) genetically engineered mouse models of pancreatic cancer using mass spectrometry proteomics. Our assessment at early-, mid-, and late-stage disease reveals an increased abundance of nidogen-2 (NID2) in the KPC model compared to KP^flC, with further validation showing that NID2 is primarily expressed by cancer-associated fibroblasts (CAFs). Using biomecha

SUBMITTER: Pereira BA 

PROVIDER: S-EPMC11221519 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature