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Gene expression profiling of MYC inducible murine tumor models (tissues) [microarray]

ABSTRACT: The transcription factor, c-MYC, is a proto-oncogene that is activated in many types of cancer. To study how MYC promotes and maintains the neoplastic phenotype, we use tetracycline-regulated systems in transgenic mice whereby we can conditionally activate MYC. We profile the changes in gene expression when MYC is activated versus inactivated in order to identify a gene signature that is associated with the ability of MYC to promote tumorigenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE143253 | GEO | 2022/10/18

REPOSITORIES: GEO

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Gene expression profiling of MYC inducible murine tumor models (cell lines) [microarray]

Project description:The transcription factor, c-MYC, is a proto-oncogene that is activated in many types of cancer. To study how MYC promotes and maintains the neoplastic phenotype, we use tetracycline-regulated systems in transgenic mice whereby we can conditionally activate MYC. We profile the changes in gene expression when MYC is activated versus inactivated in order to identify a gene signature that is associated with the ability of MYC to promote tumorigenesis.

2022-10-18 | GSE143250 | GEO

Transcription profiling of liver from mice with constitutively active Hypoxia Inducible Factor (HIF-1a and HIF-2a) or inactivated von Hippel-Lindau tumor suppressor gene product (pVHL)

Project description:The effects of constitutively active Hypoxia Inducible Factor (HIF) and inactivated von Hippel-Lindau tumor suppressor gene product (pVHL) were examined in a mouse model. Conditionally expressed, constitutively active HIF-1a and HIF-2a were compared with inactivated pVHL.

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Hippo signaling instructs ectopic but not normal organ growth [Liver YapHyper]

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MM samples for epigenomic translocation of H3K4me3 broad domains following super-enhancer hijacking

Project description:Chromosomal translocations are important drivers of haematological malignancies whereby proto-oncogenes are activated by juxtaposition with super-enhancers, often called enhancer hijacking. To examine this phenomenon we used ChipSeq based on a combination of six histone modifications as follows: H3K4me1, H3K4me3, H3K9me3, H3K27me3, H3K27Ac and H3K36me3. Samples are patient-derived xenografts generated by passaging primary patient CD138+ selected cells through the SCID-rab myeloma mouse model.

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Epigenomic translocation of H3K4me3 broad domains following super-enhancer hijacking

Project description:Chromosomal translocations are important drivers of haematological malignancies whereby proto-oncogenes are activated by juxtaposition with super-enhancers, often called super-enhancer hijacking. We analysed the epigenomic consequences of rearrangements between the enhancers of the immunoglobulin heavy chain locus (IGH) and proto-oncogene CCND1 that are common in B-cell malignancies. By integrating BLUEPRINT epigenomic data with DNA breakpoint detection, we characterised the normal chromatin landscape of the human IGH locus and its dynamics after pathological genomic rearrangement. We detected an H3K4me3 broad domain (BD) within the IGH locus of healthy B-cells that was absent in samples with IGH-CCND1 translocations. The appearance of H3K4me3-BD over CCND1 in the latter was associated with overexpression and extensive chromatin accessibility of this locus. We observed similar cancer-specific H3K4me3-BDs associated with super-enhancer hijacking of other common oncogenes in B-cell (MAF, MYC and FGFR3) and in T-cell malignancies (LMO2, TLX3 and TAL1). Our analysis suggests that H3K4me3-BDs are created by super-enhancers and supports the new concept of epigenomic translocation, where the relocation of H3K4me3-BDs accompanies the translocation of super-enhancers.

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Global analysis of RNA-binding proteins identifies a positive feedback loop between LARP1 and MYC that promotes tumorigenesis

Project description:In addition to genomic alterations, aberrant changes in post-transcriptional regulation can modify gene function and drive cancer development. RNA-binding proteins (RBPs) are a large class of post-transcriptional regulators that have been increasingly implicated in carcinogenesis. By integrating multi-omics data, we identify LARP1 as one of the most upregulated RBPs in colorectal cancer (CRC), and demonstrate its oncogenic properties. We perform LARP1:RNA interactome profiling and unveil a previously unexplored role for LARP1 in targeting the 3′UTR of oncogenes in CRC. Notably, we identify the proto-oncogenic transcription factor MYC as a key LARP1-regulated target. Our data show that LARP1 positively modulates MYC expression by associating with its 3′UTR. In addition, antisense oligonucleotide-mediated blocking of the interaction between LARP1 and the MYC 3′UTR reduces MYC expression and in vitro CRC growth. Furthermore, a systematic analysis of LARP1:protein interactions reveals IGF2BP3 and YBX1 as LARP1-interacting proteins that also regulate MYC expression and CRC development. Finally, we demonstrate that MYC reciprocally modulates LARP1 expression by targeting its enhancer. In summary, our data reveal a critical, previously uncharacterized role of LARP1 in promoting CRC tumorigenesis, validate its direct regulation of the proto-oncogene MYC, and delineate a model of the positive feedback loop between MYC and LARP1 that promotes CRC growth and development.

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Label-free whole cell proteomics for oncogene cell lines

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