Epigenomic profiling of Non-small-cell Lung Cancer (NSCLC) cells with or without Eed

ABSTRACT: Polycomb repressive complexes (PRC) are frequently implicated in human cancer acting either as oncogenes or tumor suppressors. Here we show that PRC2 is a critical regulator of Kras-driven non-small-cell lung cancer (NSCLC) progression. Modulation of PRC2 by either Ezh2 overexpression or Eed deletion enhances Kras-driven adenomagenesis and inflammation, respectively. Eed-loss-driven inflammation leads to massive macrophage recruitment and marked decline in tissue function. Additional Trp53 inactivation activates a cell autonomous epithelial-to-mesenchymal transition (EMT) program leading to an invasive mucinous adenocarcinoma. A switch between methylated/acetylated chromatin underlies the tumor phenotypic evolution, prominently involving genes controlled by Hippo/Wnt-signaling. Our observa

ORGANISM(S): Homo sapiens

SUBMITTER: Gaetano Gargiulo 

PROVIDER: E-GEOD-61190 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress