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Expression data from mouse adult fibroblasts with Rb deletion and/or p53DD expression exposed to cisplatin (CDDP)

ABSTRACT: The RB and p53 tumor suppressor pathways regulate the transcription of genes involved in cell cycle progression, DNA replication, DNA repair, and apoptosis. These tumor suppressors are critical modulators of the response to genotoxic damage and both pathways are frequently inactivated in human cancers. We used microarrays to monitor gene expression patterns upon exposure to cisplatin treatment in fibroblasts harboring loss/inactivation of RB and/or p53. We generated mouse adult fibroblasts harboring loss/inactivation of RB and/or p53 and subjected these cell populations to cisplatin treatment for 24 hours. Treated cell populations were allowed to recover from cisplatin exposure, generating a recurred cell popuation. Untreated and recurred cell populations were then subjected to RNA extraction and hybridization on Affymetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Erik Knudsen

PROVIDER: E-GEOD-18395 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from mouse adult fibroblasts with Rb deletion and/or p53DD expression exposed to cisplatin (CDDP)

Project description:The RB and p53 tumor suppressor pathways regulate the transcription of genes involved in cell cycle progression, DNA replication, DNA repair, and apoptosis. These tumor suppressors are critical modulators of the response to genotoxic damage and both pathways are frequently inactivated in human cancers. We used microarrays to monitor gene expression patterns upon exposure to cisplatin treatment in fibroblasts harboring loss/inactivation of RB and/or p53.

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Expression data of untreated or cisplatin-treated wildtype or Rb-/- MEFs

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Transcription profiling of mouse wildtype or Rb-/- MEFs treated with cisplatin vs. control

Project description:The absence of the Rb tumor suppressor gene changes levels/activities of transcription factors (e.g., E2F and p53) which alter gene expression patterns, related to cell cycle control and cellular response to DNA damage. Cisplatin is a genotoxic chemotherapeutic agent and wildtype or Rb null cells have different sensitivities to cisplatin-induced cytotoxicity. We used microarrays to compare global profiles of gene expression and distinct responses of wildtype and Rb null MEFs in response to cisplatin. Experiment Overall Design: Primary wildtype or Rb null MEFs were generated from embryos at embryonic day 13.5 and cultured to passage 2. Wildtype or Rb null MEFs were either untreated or treated with 16 microM cisplatin for 24 hours prior to harvest and RNA extraction. Four different RNA samples (wildtype or Rb-/- MEFs, untreated or cisplatin-treated) were used for hybridization in triplate to Affimatrix Chips. Then, the total of 12 hybridizations were divided into 4 subseries: UT-Rb, UT-WT, CP-Rb, CP-Wt, and each subseries contained three samples (hybridization 1-3 or a-c).

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CDDP treated KYSE140

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Genomic profiles of mouse liver tissue harboring deletion of RB and/or p53, untreated or post-hepatocarcinogen treatment [CGH data]

Project description:The retinoblastoma (RB) and p53 tumor suppressors are critical regulators of the cell cycle with profound impact on both normal cell biology and disease etiology. In the context of human cancers, compound inactivation of RB and p53 is a frequent occurrence; however, the cooperation of these tumor suppressors in driving tumorigenesis has proven to be intricate and dependent on both the tissue and type of cancer. Hepatocellular carcinoma (HCC) is a highly complex disease characterized by numerous molecular abnormalities (e.g. p53, RB, TGFβ) and chromosomal aberrations associated with environmental factors (e.g. Hepatitis B/C Virus, Aflatoxin B1). Despite extensive research, how each of these facets of disease development cooperates in promoting tumorigenesis is ultimately unknown. In the current study, we present a mouse model of liver tumorigenesis, in which the impact of RB and p53 loss is modified by the tissue environment. While loss of RB and p53 promotes deregulation of transcriptional programs associated with advanced disease, these changes are not sufficient to drive spontaneous tumorigenesis in the liver. However, in response to carcinogen-induced damage, distinct and cooperative roles of RB and p53 are revealed, which critically impact cell cycle control, checkpoint response, genome stability, and ultimately tumor development. Mice that are transgenic for Cre recombinase under the albumin promoter and harboring loxP sites within the Rb and/or p53 genes. For gene expression microarray analysis, mice were aged to 14 days, and treated for 24 hours with diethylnitrosamine (DEN) or saline as a control. For CGH analysis, mice were aged to 6 months post-DEN treatment. Liver tissue was obtained from dissected tumors and compared to normal liver tissue of 6-month old, saline-treated littermates. CGH analysis includes 5 individual tumor samples and 2 control samples (each consisting of a pool of 3 normal mouse liver DNA).

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Gene expression profiles of mouse liver tissue harboring deletion of RB and/or p53, untreated or post-hepatocarcinogen treatment

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