Loss of Cadherin-11 in pancreatic ductal adenocarcinoma alters tumor-immune microenvironment.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is one of the top five deadliest forms of cancer with very few treatment options. The 5-year survival rate for PDAC is 10% following diagnosis. Cadherin 11 (Cdh11), a cell-to-cell adhesion molecule, has been suggested to promote tumor growth and immunosuppression in PDAC, and Cdh11 inhibition significantly extended survival in mice with PDAC. However, the mechanisms by which Cdh11 deficiency influences PDAC progression and anti-tumor immune responses have yet to be fully elucidated. To investigate Cdh11-deficiency induced changes in PDAC tumor microenvironment (TME), we crossed p48-Cre; LSL-Kras^G12D/+; LSL-Trp53^R172H/+ (KPC) mice with Cdh11^+/- mice and performed single-cell RNA sequencing (scRNA-s

SUBMITTER: Sebastian A 

PROVIDER: S-EPMC10639148 | biostudies-literature | 2023

REPOSITORIES: biostudies-literature