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P53 In Inflamatory Stress Response


ABSTRACT: Activation of the p53 network plays a central role in the inflammatory stress response associated with ulcerative colitis, and may modulate cancer risk in patients afflicted with this chronic disease. The overall goal of these experiments is to study the gene expression profiles associated with four microenvironmental components of the inflammatory response (NO*, DNA damage, DNA replication arrest, and hypoxia) that result in p53 stabilization and activation. To this end, isogenic HCT116 and HCT116 TP53-/- colon cancer cells were exposed to the NO*-donor Sper/NO, H2O2 (DNA damage), hypoxia, or hydroxyurea (HU, DNA replication arrest), and their mRNA was analyzed using oligonucleotide microarrays. Cy3-labeled reference probes (untreated) and Cy5-labeled probes (samples exposed for the indicated times) were hybridized to 70-mer oligonucleotide microarrays with 21,329 probes (Qiagen Human Array-Ready Oligo Set, Version 2.0). The arrays were printed by the Advanced Technology Center at the National Cancer Institute. At least two hybridizations (range 2-5) were performed for each sample.

ORGANISM(S): Homo sapiens

SUBMITTER: Ana Robles 

PROVIDER: E-GEOD-3176 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

The p53 tumor suppressor network is a key responder to microenvironmental components of chronic inflammatory stress.

Staib Frank F   Robles Ana I AI   Varticovski Lyuba L   Wang Xin W XW   Zeeberg Barry R BR   Sirotin Michail M   Zhurkin Victor B VB   Hofseth Lorne J LJ   Hussain S Perwez SP   Weinstein John N JN   Galle Peter R PR   Harris Curtis C CC  

Cancer research 20051101 22


Activation of the p53 network plays a central role in the inflammatory stress response associated with ulcerative colitis and may modulate cancer risk in patients afflicted with this chronic disease. Here, we describe the gene expression profiles associated with four microenvironmental components of the inflammatory response (NO*, H2O2, DNA replication arrest, and hypoxia) that result in p53 stabilization and activation. Isogenic HCT116 and HCT116 TP53-/- colon cancer cells were exposed to the N  ...[more]

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