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Gene Expression profiling of Myc-induced lymphomagenesis

ABSTRACT: The ability of oncogenes to provoke cancer is harnessed by regulators that control cell proliferation or induce apoptosis, and bypass of these checkpoints is a hallmark of malignancies. Myc oncoproteins are overexpressed in ~70% of all cancers and induce numerous transcription targets that regulate cell growth, metabolism, and the ribosome machinery. We used the Eμ-Myc mouse model from which one can directly compare expression profiles of wild type versus Myc-expressing B220+ pre-malignant lymphocytes and also queried differences in gene expression that ensue following the neoplastic switch to lymphoma (Nilsson et al., 2005 - PMID:15894264 and Keller et al. 2010 - PMID:20598117).

ORGANISM(S): Mus musculus

PROVIDER: GSE32239 | GEO | 2011/10/31

SECONDARY ACCESSION(S): PRJNA147195

REPOSITORIES: GEO

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Gene Expression profiling of Myc-induced lymphomagenesis

Project description:The ability of oncogenes to provoke cancer is harnessed by regulators that control cell proliferation or induce apoptosis, and bypass of these checkpoints is a hallmark of malignancies. Myc oncoproteins are overexpressed in ~70% of all cancers and induce numerous transcription targets that regulate cell growth, metabolism, and the ribosome machinery. We used the Eμ-Myc mouse model from which one can directly compare expression profiles of wild type versus Myc-expressing B220+ pre-malignant lymphocytes and also queried differences in gene expression that ensue following the neoplastic switch to lymphoma (Nilsson et al., 2005 - PMID:15894264 and Keller et al. 2010 - PMID:20598117). Wild type and precancerous Eμ-Myc transgenic B cells (from 4-6 week old littermates), and lymphomas from 13 independent Eμ-Myc mice were investigated. These samples were used for subsequent RNA purification, labeling and hybridization to MOE430A Affymetrix arrays.

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DNMT3B7 disrupts embryonic development and accelerates lymphomagenesis

Project description:Cancer cells have an altered distribution of DNA methylation and express aberrant DNA methyltransferase 3B transcripts, which encode truncated proteins. To test if a truncated DNMT3B isoform disrupts DNA methylation in vivo, we constructed transgenic mice expressing DNMT3B7, a common truncated DNMT3B isoform in cancer cells. DNMT3B7 transgenic mice exhibit altered embryonic development, including lymphopenia, craniofacial abnormalities, and cardiac defects, similar to Dnmt3b-deficient animals, but rarely develop cancer. However, DNMT3B7 expression increases the frequency of mediastinal lymphomas in Eμ−myc animals. Eμ-myc/DNMT3B7 lymphomas have more chromosomal rearrangements, increased global methylation levels, and more locus-specific perturbations in DNA methylation patterns compared to Eμ-myc lymphomas. Our results demonstrate that a truncated DNMT3B protein can alter tumorigenesis, suggesting a similar role in human tumors. Direct comparison of DNA methylation in lymphoma samples from Eu-Myc vs Eu-Myc/Dnmt3b7 mice.

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Project description:'The REL gene, encoding the NF-κB subunit c-Rel, is frequently amplified in B-cell lymphoma and functions as a tumour promoting transcription factor. Here we report the surprising result that c-rel -/- mice display significantly earlier lymphomagenesis in the c-Myc driven, Eμ-Myc model of B-cell lymphoma. c-Rel loss also led to earlier onset of disease in a separate TCL1-Tg driven lymphoma model. Tumour reimplantation experiments indicated that this is an effect intrinsic to the Eμ-Myc lymphoma cells but, counter-intuitively, c-rel -/- Eμ-Myc lymphoma cells were more sensitive to apoptotic stimuli. To learn more about why loss of c-Rel led to earlier onset of disease, microarray gene expression analysis was performed on B-cells from 4-week old, wild type and c-rel -/- Eμ-Myc mice. Extensive changes in gene expression were not seen at this age but among those transcripts significantly downregulated by the loss of c-Rel was the B-cell tumour suppressor BTB and CNC homology 2 (Bach2). Q-PCR and western blot analysis confirmed loss of Bach2 in c-Rel mutant Eμ-Myc tumours at both 4 weeks and the terminal stages of disease. Moreover Bach2 expression was also downregulated in c-rel -/- TCL1-Tg mice and RelA Thr505Ala mutant Eμ-Myc mice. Analysis of wild type Eμ-Myc mice demonstrated that the population expressing low levels of Bach2 exhibited the earlier onset of lymphoma seen in c-rel-/- mice. Confirming the relevance of these findings to human disease, analysis of ChIP-Seq data revealed that Bach2 is a c-Rel and NF-κB target gene in transformed human B-cells, while treatment of Burkitt''s lymphoma cells with inhibitors of the NF-κB/IKK pathway or deletion of c-Rel or RelA resulted in loss of Bach2 expression. This data reveals a surprising tumour suppressor role for c-Rel in lymphoma development explained by regulation of Bach2 expression, underlining the context dependent complexity of NF-κB signalling in cancer.'

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DNMT3B7 disrupts embryonic development and accelerates lymphomagenesis

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rDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [4C-seq]

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