Expression data from proliferating and senescent murine hepatic stellate cells

ABSTRACT: The p53 protein is a cell-autonomous tumor suppressor that restricts malignant transformation by triggering cell cycle exit or apoptosis. p53 also promotes cellular senescence, a program that triggers a stable cell cycle arrest and can modify the tissue microenvironment through its effect on cell membrane and secretory proteins. Here we show that specific ablation of p53 in hepatic stellate cells, which undergo a process of proliferation and senescence in the fibrogenic response to liver damage, enhances liver cirrhosis, reduces survival and increases the malignant transformation of adjacent epithelial cells into hepatocellular carcinoma. This p53-dependent senescence program involves the release of secreted proteins which skew macrophages into a tumor-inhibiting M1-state that can eliminat

ORGANISM(S): Mus musculus

SUBMITTER: Amaia Lujambio 

PROVIDER: E-GEOD-39469 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress