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The hijack of a cellular failsafe program at the initiation of colorectal cancers.

ABSTRACT: The aim of this study was to set up an in vitro model to highlight yet-unidentified mechanisms facilitating the escape of human colonic epithelial cells from chronic inflammation-induced senescence, and to define whether these mechanisms afford cells a resistance to oxidative stress thereby contributing to tumor initiation. By driving a specific genetic program (termed ALEP), as observed in ulcerative colitis and Crohn’s disease patients, transient expression of ZEB transcription factors buffers ROS deleterious effects and maintains intestinal stem cell (ISC) integrity. Nonetheless, as a perverse effect, maintenance of this program is likely to facilitate their neoplastic transformation and contribute to tumor initiation. We identified the quinolinate phosphoribosyltransferase enzyme (QPRT) as the main component of the ALEP-associated survival advantage. Here is mRNA expression data of second cohort of 50 sporadic primary colorectal carcinomas (CRC) resected from untreated patients used in conjunction with their QPRT values assessed by IHC. These 50 CRCs were scored for ALEP, Stem-like, Lgr5 and EphB2high signatures to test correlation with QPRT.

ORGANISM(S): Homo sapiens

SUBMITTER: Louise Hill

PROVIDER: E-MTAB-4090 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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