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Mouse HCC model

ABSTRACT: A mouse model of HCC has been developed based on the reported inactivation of the RB pathway in the majority of human HCC. This mouse model harbors floxed alleles of Rb and p130 genes, as well as germline mutation of the p107 gene. Various strategies to activate the activity of a Cre recombinase leads to the efficient deletion of the three genes in the liver of adult mice (TKO mice). Disruption of the RB pathway induces the rapid development of HCC. These HCCs share many similar features of human HCC. The goal of this array is to assess genome wide expression of TKO HCCs. Gene expression of control livers (n=4) or TKO HCCs (n=5) was measured using the Affymetrix GeneChip Mouse Genome 430-2.0 arrays

ORGANISM(S): Mus musculus

SUBMITTER: Patrick Viatour

PROVIDER: E-GEOD-19004 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Notch signaling inhibits hepatocellular carcinoma following inactivation of the RB pathway.

Viatour Patrick P Ehmer Ursula U Saddic Louis A LA Dorrell Craig C Andersen Jesper B JB Lin Chenwei C Zmoos Anne-Flore AF Mazur Pawel K PK Schaffer Bethany E BE Ostermeier Austin A Vogel Hannes H Sylvester Karl G KG Thorgeirsson Snorri S SS Grompe Markus M Sage Julien J

The Journal of experimental medicine 20110829 10

Hepatocellular carcinoma (HCC) is the third cancer killer worldwide with >600,000 deaths every year. Although the major risk factors are known, therapeutic options in patients remain limited in part because of our incomplete understanding of the cellular and molecular mechanisms influencing HCC development. Evidence indicates that the retinoblastoma (RB) pathway is functionally inactivated in most cases of HCC by genetic, epigenetic, and/or viral mechanisms. To investigate the functional relevan ...[more]

PMID: 21875955

Similar Datasets

Mouse HCC model

Project description:A mouse model of HCC has been developed based on the reported inactivation of the RB pathway in the majority of human HCC. This mouse model harbors floxed alleles of Rb and p130 genes, as well as germline mutation of the p107 gene. Various strategies to activate the activity of a Cre recombinase leads to the efficient deletion of the three genes in the liver of adult mice (TKO mice). Disruption of the RB pathway induces the rapid development of HCC. These HCCs share many similar features of human HCC.

2010-07-01 | GSE19004 | GEO

Gene expression profile of the V/SVZ and the CP at E16

Project description:Cell differentiation and proliferation are mutually exclusive. Although differentiating neurons are recognized as post-mitotic non-dividing cells, some Rb- and Rb family (Rb, p107, and p130)-deficient differentiating neurons proliferate and form tumor. Here, we found that the acute inactivation of all Rb family in differentiating cortical excitatory neurons caused radial migration defect and S-phase progression but not cell division, whereas that in cortical progenitors caused the cell division of the differentiating neurons generated from Rb â??/â??; p107 â??/â??; p130 â??/â?? (Rb-TKO) progenitors. Genome-wide DNA methylation analysis revealed that proximal promoters tended to become methylated during differentiation in vivo. DNA demethylation by DNA methyltransferase inhibitor allowed the acutely inactivated Rb-TKO differentiating neurons to undergo G2/M-phase progression. Our finding illustrate that cortical excitatory neurons epigenetically lose their proliferative potency after neurogenesis. 4 samples of the V/SVZ (ventricular/subventricular zone) tissue and 4 samples of the CP (cortical plate) tissue

2016-07-03 | E-GEOD-37576 | biostudies-arrayexpress

Gene expression profile of cerebral cortical cells after Rb family inactivation in progenitors and neurons

Project description:Cell cycle deregulation leads to abnormal proliferation and cell death in a context-specific manner. Cell cycle progression driven via Rb pathway forces neurons to undergo S-phase, resulting in cell death associated with the progression of neuronal degeneration. Nevertheless, some Rb- and Rb family (Rb, p107, and p130)-deficient differentiating neurons can proliferate and form tumors. Here, we found that differentiating cerebral cortical excitatory neurons underwent S-phase progression but not cell division after acute Rb family inactivation in differentiating neurons. However, the differentiating neurons underwent cell division and form tumors when Rb family members were inactivated in cortical progenitors. Differentiating neurons generated from Rb -/-; p107 -/-; p130 -/- (Rb-TKO) progenitors, but not acutely inactivated Rb-TKO differentiating neurons, activated DNA double-strand break (DSB) repair pathway without increasing the tri-methylation of histone H4 at lysine 20 (H4K20M3), which is known to protect from DNA damage. The activation of DSB repair pathway was essential for the cell division of Rb-TKO differentiating neurons. These results suggest that newly-born cortical neurons from progenitors epigenetically become protected from DNA damage and cell division in a Rb family-dependent manner. 3 samples of pCAG-control, pCAG-RbTKO, pMAP2-control, and pMAP2-RbTKO cells

2014-01-01 | E-GEOD-37577 | biostudies-arrayexpress

Gene expression profile of the V/SVZ and the CP at E16

Project description:Cell differentiation and proliferation are mutually exclusive. Although differentiating neurons are recognized as post-mitotic non-dividing cells, some Rb- and Rb family (Rb, p107, and p130)-deficient differentiating neurons proliferate and form tumor. Here, we found that the acute inactivation of all Rb family in differentiating cortical excitatory neurons caused radial migration defect and S-phase progression but not cell division, whereas that in cortical progenitors caused the cell division of the differentiating neurons generated from Rb –/–; p107 –/–; p130 –/– (Rb-TKO) progenitors. Genome-wide DNA methylation analysis revealed that proximal promoters tended to become methylated during differentiation in vivo. DNA demethylation by DNA methyltransferase inhibitor allowed the acutely inactivated Rb-TKO differentiating neurons to undergo G2/M-phase progression. Our finding illustrate that cortical excitatory neurons epigenetically lose their proliferative potency after neurogenesis.

2016-01-01 | GSE37576 | GEO

MBD-Seq of the V/SVZ and the CP at E16

Project description:Cell differentiation and proliferation are mutually exclusive. Although differentiating neurons are recognized as post-mitotic non-dividing cells, some Rb- and Rb family (Rb, p107, and p130)-deficient differentiating neurons proliferate and form tumor. Here, we found that the acute inactivation of all Rb family in differentiating cortical excitatory neurons caused radial migration defect and S-phase progression but not cell division, whereas that in cortical progenitors caused the cell division of the differentiating neurons generated from Rb –/–; p107 –/–; p130 –/– (Rb-TKO) progenitors. Genome-wide DNA methylation analysis revealed that proximal promoters tended to become methylated during differentiation in vivo. DNA demethylation by DNA methyltransferase inhibitor allowed the acutely inactivated Rb-TKO differentiating neurons to undergo G2/M-phase progression. Our finding illustrate that cortical excitatory neurons epigenetically lose their proliferative potency after neurogenesis.

2014-01-01 | GSE37601 | GEO

Mouse small cell lung cancer model

Project description:A mouse model for human small cell lung carcinoma (SCLC) has been developed based on evidence in human tumors that the tumor suppressor functions of RB and p53 are defective in more than 90% of SCLC cases. We also developed another mouse model also combines loss of p130 (Rbl2), an RB-related gene, with deletion of RB and p53. These two mouse tumors were shown to closely resemble human SCLC. The goal of this array experiment is to assess genome-wide gene expression of those mouse tumors and determine the similarity of the mouse models to human SCLC. Gene expression from Mouse Rb/p53 ( n=10 ) and Rb/p53/p130 primary tumors ( n=3 ) as well as tumor-free adult mouse lungs ( n=2 ) was measured using the Affymetrix GeneChip Mouse Genome 430-2.0 arrays.

2010-06-08 | E-GEOD-18534 | biostudies-arrayexpress

MBD-Seq of the V/SVZ and the CP at E16

Project description:Cell differentiation and proliferation are mutually exclusive. Although differentiating neurons are recognized as post-mitotic non-dividing cells, some Rb- and Rb family (Rb, p107, and p130)-deficient differentiating neurons proliferate and form tumor. Here, we found that the acute inactivation of all Rb family in differentiating cortical excitatory neurons caused radial migration defect and S-phase progression but not cell division, whereas that in cortical progenitors caused the cell division of the differentiating neurons generated from Rb –/–; p107 –/–; p130 –/– (Rb-TKO) progenitors. Genome-wide DNA methylation analysis revealed that proximal promoters tended to become methylated during differentiation in vivo. DNA demethylation by DNA methyltransferase inhibitor allowed the acutely inactivated Rb-TKO differentiating neurons to undergo G2/M-phase progression. Our finding illustrate that cortical excitatory neurons epigenetically lose their proliferative potency after neurogenesis. 1 sample of the V/SVZ tissue and the CP tissue

2014-01-01 | E-GEOD-37601 | biostudies-arrayexpress

Gene expression profile of cerebral cortical cells after Rb family inactivation in progenitors and neurons

2014-01-01 | GSE37577 | GEO

Transcription profiling of mouse Rb family triple knock-out (TKO) embryonic stem cells as they differentiate in vivo

Project description:The retinoblastoma cell cycle regulator pRb and the two related proteins p107 and p130 are thought to suppress cancer development both by inhibiting the G1/S transition of the cell cycle in response to growth-arrest signals and by promoting cellular differentiation. Here, we investigated the phenotype of Rb family triple knock-out (TKO) embryonic stem cells as they differentiate in vivo and in culture. Confirming the central role of the Rb gene family in cell cycle progression, TKO mouse embryos did not survive past mid-gestation and differentiating TKO cells displayed increased proliferation and cell death. However, patterning and cell fate determination were largely unaffected in these TKO embryos. Furthermore, a number of TKO cells, including in the neural lineage, were able to exit the cell cycle in G1 and terminally differentiate. This ability of Rb family TKO cells to undergo cell cycle arrest was associated with the repression of target genes for the E2F6 transcription factor, uncovering a pRb-independent control of the G1/S transition of the cell cycle. These results show that the Rb gene family is required for proper embryonic development but is not absolutely essential to induce G1 arrest and differentiation in certain lineages. Experiment Overall Design: Genome-wide gene expression was analyzed for wild-type and TKO ESC and EB cells. Three biological replicates were isolated for wild-type ESCs, TKO ESCs, and wild-type EBs, while five biological replicates were isolated for TKO EBs.

2009-09-12 | E-GEOD-13408 | biostudies-arrayexpress

Transcription profiling of mouse epidermis from Rb(F19/F19)K14cre;Rbl2-/- (pRb-;p130-) mutants to analyse functional redundancies between retinoblastoma family members

Project description:The epidermal-specific ablation of Rb gene leads to increased proliferation, aberrant differentiation, and the disengagement of these processes in vivo and in vitro. These differences in phenotype are more severe with the loss of p107, demonstrating the functional compensation between pRb and p107. As p107 and p130 also exert overlapping functions in epidermis, we have generated Rb(F19/F19)K14cre;Rbl2-/- (pRb-;p130-) mice to analyze possible functional redundancies between pRb and p130. The epidermal phenotype was very similar between pRb- and pRb-;p130- mice, suggesting that pRb and p130 activities are not redundant in epidermis. Importantly, we can correlate the proliferation differences with specific changes in gene expression between pRb-, pRb-;p107- and pRb-;p130- primary keratinocytes using microarray analysis, and explain the phenotypes in the context of altered E2F expression and functionality. Our findings support a model in which the distinct retinoblastoma family members, in conjunction with E2F members, play a central role in regulating epidermal homeostasis through specific or overlapping activities. Experiment Overall Design: Total RNA from pooled cells from each genotype were analyzed, per duplicate (pRb-/-;p107-/-, or pRb-/-;p130-/-) or triplicate (wild type, or pRb-/-), in mouse microarrays. Comparison was performed between the 4 different genotypes.

2008-06-16 | E-GEOD-9562 | biostudies-arrayexpress

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