Activation of PPARγ in Myeloid Cells Promotes Progression of Epithelial Lung Tumors through TGFβ1.

ABSTRACT: Lung cancer is a heterogeneous disease in which patient-specific treatments are desirable and the development of targeted therapies has been effective. Although mutations in KRAS are frequent in lung adenocarcinoma, there are currently no targeted agents against KRAS. Using a mouse lung adenocarcinoma cell line with a Kras mutation (CMT167), we previously showed that PPARγ activation in lung cancer cells inhibits cell growth in vitro yet promotes tumor progression when activated in myeloid cells of the tumor microenvironment. Here, we report that PPARγ activation in myeloid cells promotes the production of TGFβ1, which, in turn, acts on CMT167 cancer cells to increase migration and induce an epithelial-mesenchymal transition (EMT). Targeting TGFβ1 signaling in CMT167 c

SUBMITTER: Sippel TR 

PROVIDER: S-EPMC7439607 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature