Regulation of GLI underlies a role for BET bromodomains in pancreatic cancer growth and the tumor microenvironment

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is extraordinarily chemoresistant and the abundant stromal content of these tumors contributes to the ineffective treatment of this disease. While the genetic alterations of PDAC have been well characterized, the epigenetic pathways regulating PDAC remain, for the most part, elusive. Employing an in vivo shRNA screen targeting epigenetic regulators, we identified members of the BET family of chromatin adaptors as key regulators of PDAC cell growth and maintenance of the tumor stroma. BET family members contribute to PDAC cell growth by modulating the activity of two key transcriptional programs, MYC and GLI. Within the cancer cells, BET inhibition also results in down-regulation of a key mediator of the tumor microenvironment, SHH, corresponding

ORGANISM(S): Homo sapiens

SUBMITTER: Andrew Liss 

PROVIDER: E-GEOD-55209 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress