Regulation of ROS signaling by TIGAR induces cancer-modulating responses in the tumor microenvironment.

ABSTRACT: The consequences of reactive oxygen species (ROS) in cancer cells are complex and have been shown to both promote and retard tumorigenesis in different models. In mouse models of pancreatic ductal adenocarcinoma (PDAC), loss of the antioxidant defense gene Tigar results in both a reduction in the development of early pancreatic intraepithelial neoplasia and an increase in invasive and metastatic capacity, accompanied by decreased survival of mice lacking pancreatic TIGAR. We previously demonstrated that increased ROS following loss of TIGAR promotes various cancer cell-intrinsic changes that contribute to metastatic capacity, including epithelial to mesenchymal transition, enhanced migration and invasion, and an increase in ERK signaling. In this study, we show that pancreatic overe

SUBMITTER: Cheung EC 

PROVIDER: S-EPMC11648893 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature