Sox9 controls self-renewal of oncogene targeted cells and links tumor initiation and invasion [ChIP-Seq]

ABSTRACT: Sox9 is a transcription factor expressed in most solid tumors. However, the molecular mechanisms underlying Sox9 function during tumorigenesis remain unclear. Here, using a genetic mouse model of basal cell carcinoma (BCC), the most frequent cancer in human, we show that Sox9 is expressed from the earliest step of tumor formation in a Wnt/β-catenin dependent manner. Deletion of Sox9 together with the constitutive activation of Hedgehog (HH) signaling completely prevents BCC formation and leads to a progressive loss of oncogene expressing cells. Transcriptional profiling of oncogene expressing cells with Sox9 deletion, combined with in vivo ChIP-sequencing uncovers a cancer-specific gene network regulated by Sox9 that promotes stemness, extracellular matrix (ECM) deposition and cytoskeleton

ORGANISM(S): Mus musculus

SUBMITTER: Jean-Christophe Larsimont 

PROVIDER: E-GEOD-68755 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress