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Gene expression of E2f7/8/Rb1 triple mutant liver tumors

ABSTRACT: Gene expression of E2f7/8/Rb1 triple mutant liver tumors

PROVIDER: PRJNA723582 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14295200.fastq.gz	Fastqsanger.gz
	SRR14295201.fastq.gz	Fastqsanger.gz
	SRR14295202.fastq.gz	Fastqsanger.gz
	SRR14295203.fastq.gz	Fastqsanger.gz
	SRR14295204.fastq.gz	Fastqsanger.gz

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Gene expression of E2f7/8/Rb1 triple mutant liver tumors

Project description:E2F-transcription factors activate many genes involved in cell cycle progression, DNA repair, and apoptosis. Hence, E2F-dependent transcription must be tightly regulated to prevent tumorigenesis, and therefore metazoan cells possess multiple E2F regulation mechanism. The best-known is the Retinoblastoma protein (RB), which is mutated in many cancers. Atypical E2Fs (E2F7 and -8) can repress E2F-target gene expression independently of RB and are rarely mutated in cancer. Therefore, they may act as emergency brakes in RB-mutated cells to suppress tumor growth. Currently it is unknown if and how RB and atypical E2Fs functionally interact in vivo. Here, we demonstrate that mice with liver-specific combinatorial deletion of Rb and E2f7/8 have reduced life spans compared to E2f7/8 or Rb deletion alone. This was associated with increased proliferation and enhanced malignant progression of liver tumors. Hence, atypical repressor E2Fs and RB cooperatively act as tumor suppressors in hepatocytes. We propose that the complex interactions between atypical E2Fs and RB on maintenance of genetic stability underlie this context-dependency.

2021-04-22 | GSE172508 | GEO

Transcription profiling of mouse Rb1 deficient Apc1638N cecal tumors vs duodenal tumors

Project description:To examine the role of Rb1 in gastrointestinal (GI) tumors we generated mice with an Apc1638N allele, Rbtm2brn floxed alleles, and a villlin-cre transgene (RBVCA). These mice had reduced median survival due to an increase in tumor incidence and multiplicity in the cecum and the proximal colon; they differed from murine intestinal tumors of the Apc1638N type which normally arise solely in the small intestine. We have examined by micro-array analysis three cecal tumors from these mice (probable adenomas), and compared them to three duodenal tumors (probable adenocarcinomas). Expression profiles of duodenal and cecal tumors relative to each other show unique gene subsets up and down regulated. The two tumor types were subsequently shown to differentially regulate distinct sets of genes over expressed in a majority of human colorectal carcinomas. Experiment Overall Design: We have compared 3 cecal tumors with 3 duodenal tumors from Rb1 deficient Apc1638N mice.

2008-11-13 | E-GEOD-13298 | biostudies-arrayexpress

Transcriptome analysis of Chx10-Cre Rb1/p107 and Chx10-Cre Rb1/p107/Hells tumors

Project description:We used novel genetically engineered mouse models to investigate the role of HELLS during tumorigenesis. Loss of HELLS drastically decreased the incidence of retinoblastoma, delayed tumor progression, and increased overall survival. Tumors from Rb1/p107 DKO and Rb1/p107/Hells TKO mice were analyzed for gene expression using RNA-seq.

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Transcriptomes of E2F7/8 DKO liver tumors

Project description:E2F transcriptional activators and repressors regulate cell cycle-dependent gene expression. Using a series of E2f loss- and gain-of-function mice we show that development is relatively insensitive to alterations in individual E2F levels and composition. However, modest increases in E2F transcriptional output (E2f7Δ/Δ;E2f8Δ/Δ, E2f1KI/1KI and E2f3bKI/3bKI) resulted in spontaneous hepatocellular carcinoma (HCC) without additional organ involvement, whereas decreases (E2f1-/- and E2f3b-/-) protected against HCC. DNA binding domain-, cell type- and temporal-specific gene ablation strategies defined a cell autonomous oncogenic role for E2F1/3B and a tumor suppressor role for E2F8 in hepatocytes during early post-natal liver development. Chromatin binding and expression profiling revealed a mechanism involving activation by E2F1/3B and repression by E2F7/8 to antagonistically regulate a common set of target genes associated with HCC progression. Thus, while development is sufficiently robust to withstand changes in E2F composition and activity, the liver is uniquely sensitive to perturbations in E2Fs. In summary, precise E2F transcriptional output in hepatocytes during early adolescence is critical to foster a cancer-free life span.

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Targeting RABL6A-RB1 signaling suppresses malignant peripheral nerve sheath tumors

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Rb1 deficient Apc1638N cecal tumors vs duodenal tumors

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E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells

Project description:This SuperSeries is composed of the following subset Series: GSE32353: Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells (nCounter) GSE32354: Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null liver (Affymetrix) Refer to individual Series

2012-08-31 | E-GEOD-32355 | biostudies-arrayexpress

Triple Negative Breast tumors: SPARC Positive Tumors vs SPARC Negative Tumors

Project description:The aim of this study was evaluate the transcriptome changes in the comparison between triple negative tumors with increased SPARC expression and triple negative tumors with decreased SPARC expression according to Nagai et al., 2011 (Breast Cancer Res Treat (2011) 126:1–14) The results generated could be of particular interest to better define the prognostic impact of SPARC expression in triple negative breast tumors

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Murine Prostate Tissue: Rb1 null vs. Rb1 E2F binding deficient mutant

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