Macrophage-secreted MMP9 induces mesenchymal transition in pancreatic cancer cells via PAR1 activation.

ABSTRACT:

Purpose

Targeting tumor-infiltrating macrophages limits progression and improves chemotherapeutic responses in pancreatic ductal adenocarcinoma (PDAC). Protease-activated receptor (PAR)1 drives monocyte/macrophage recruitment, and stromal ablation of PAR1 limits cancer growth and enhances gemcitabine sensitivity in experimental PDAC. However, the functional interplay between PAR1, macrophages and tumor cells remains unexplored. Here we address the PAR1-macrophage-tumor cell crosstalk and assess its contributions to tumor progression.

Methods

PAR1 expression and macrophage infiltration were correlated in primary PDAC biopsies using gene expression datasets and tissue microarrays. Medium transfer experiments were used to evaluate the functional consequences of macrophage-tumor

SUBMITTER: Tekin C 

PROVIDER: S-EPMC7717035 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature