Targeting galectin-1 inhibits pancreatic cancer progression by modulating tumor-stroma crosstalk.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDA) remains one of the most lethal tumor types, with extremely low survival rates due to late diagnosis and resistance to standard therapies. A more comprehensive understanding of the complexity of PDA pathobiology, and especially of the role of the tumor microenvironment in disease progression, should pave the way for therapies to improve patient response rates. In this study, we identify galectin-1 (Gal1), a glycan-binding protein that is highly overexpressed in PDA stroma, as a major driver of pancreatic cancer progression. Genetic deletion of Gal1 in a Kras-driven mouse model of PDA (Ela-Kras^G12Vp53^-/- ) results in a significant increase in survival through mechanisms involving decreased stroma activat

SUBMITTER: Orozco CA 

PROVIDER: S-EPMC5910865 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature