Physical and functional CSL-p53 interactions underlie control of cancer stromal cell evolution [ChIP-seq]

ABSTRACT: Senescence of stromal fibroblasts has been linked to establishment of cancer associated fibroblasts (CAF) and aging-associated increase of tumors. However, in clinically occurring carcinomas, density and proliferation of CAFs are frequently increased rather than decreased. We previously showed that genetic deletion or down-modulation of the canonical Notch effector CSL/RBP-J? in skin dermal fibroblasts is sufficient for CAF activation with consequent development of multifocal keratinocyte tumors. We now show that CSL deletion or knockdown induces senescence of primary fibroblasts derived from dermis, oral mucosa, breast and lung. CSL functions in these cells as a constitutive direct repressor of multiple senescence- and CAF-effector genes. At the same time, it physically interacts with p53

ORGANISM(S): Homo sapiens

SUBMITTER: Paola Ostano 

PROVIDER: E-GEOD-59942 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress