Activation of the GPR35 pathway drives angiogenesis in the tumour microenvironment.

ABSTRACT:

Objective

Primary sclerosing cholangitis (PSC) is in 70% of cases associated with inflammatory bowel disease. The hypermorphic T108M variant of the orphan G protein-coupled receptor GPR35 increases risk for PSC and ulcerative colitis (UC), conditions strongly predisposing for inflammation-associated liver and colon cancer. Lack of GPR35 reduces tumour numbers in mouse models of spontaneous and colitis associated cancer. The tumour microenvironment substantially determines tumour growth, and tumour-associated macrophages are crucial for neovascularisation. We aim to understand the role of the GPR35 pathway in the tumour microenvironment of spontaneous and colitis-associated colon cancers.

Design

Mice lacking GPR35 on their macrophages underwent models of spontaneous colon can

SUBMITTER: Pagano E 

PROVIDER: S-EPMC8862021 | biostudies-literature | 2022 Mar

REPOSITORIES: biostudies-literature