Leukemogenesis by CDX2 involves KLF4 repression and deregulated PPARgamma signaling.

ABSTRACT: Aberrant expression of the homeodomain transcription factor CDX2 occurs in most cases of acute myeloid leukemia (AML) and promotes leukemogenesis, making CDX2, in principle, an attractive therapeutic target. Conversely, CDX2 acts as a tumor suppressor in colonic epithelium. The effectors mediating the leukemogenic activity of CDX2 and the mechanism underlying its context-dependent properties are poorly characterized, and strategies for interfering with CDX2 function in AML remain elusive. We report data implicating repression of the transcription factor KLF4 as important for the oncogenic activity of CDX2, and demonstrate that CDX2 differentially regulates KLF4 in AML versus colon cancer cells through a mechanism that involves tissue-specific patterns of promoter binding and epigenetic mod

ORGANISM(S): Mus musculus

SUBMITTER: Lars Bullinger 

PROVIDER: E-GEOD-40939 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress