Deregulation of the Ras-Erk Signaling Axis Modulates the Enhancer Landscape [RNA-seq]

ABSTRACT: Unrestrained receptor tyrosine kinase (RTK) signaling and epigenetic deregulation are root causes of tumorigenesis. We establish linkage between these processes by demonstrating that aberrant RTK signaling unleashed by oncogenic HRasG12V or loss of negative feedback through Sprouty gene deletion remodels histone modifications associated with active typical and super-enhancers. However, while both lesions disrupt the Ras-Erk axis, the expression programs, enhancer signatures, and transcription factor networks modulated upon HRasG12V-transformation or Sprouty deletion are largely distinct. Oncogenic HRasG12V elevates histone 3 lysine 27 acetylation (H3K27ac) levels at enhancers near the transcription factor Gata4 and the kinase Prkcb, as well as their expression levels. We show that Gata4 is

ORGANISM(S): Mus musculus

SUBMITTER: Behnam Nabet 

PROVIDER: E-GEOD-63497 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress