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Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional profiling of 2D colonies derived from WT, Bmi1-/-, and Bmi1-/-;Ink4a/Arf Labial cervical loops

ABSTRACT: This experiment is aimed at determining the genetic signature of dental stem cell colonies grown in vitro and how that signature changes when Bmi1 activity is removed. Another question to be answered by the experiment is whether Bmi1 has alternate targets besides Ink4a/Arf. There are 12 total samples: 4 biological replicates for each genotype that consist of single colonies grown in vitro.

ORGANISM(S): Mus musculus

SUBMITTER: Brian Biehs

PROVIDER: E-GEOD-46000 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptional profiling of 2D colonies derived from WT, Bmi1-/-, and Bmi1-/-;Ink4a/Arf Labial cervical loops

Project description:This experiment is aimed at determining the genetic signature of dental stem cell colonies grown in vitro and how that signature changes when Bmi1 activity is removed. Another question to be answered by the experiment is whether Bmi1 has alternate targets besides Ink4a/Arf.

2013-04-12 | GSE46000 | GEO

Expression data from Bmi1-overexpressing Ink4a-Arf-null hepatoblasts

Project description:Forced expression of Bmi1 accelerated the self-renewal of hepatic stem/progenitor cells and eventually induced their transformation in an in vivo transplant model. The Ink4a/Arf locus, which encodes a cyclin-dependent kinase inhibitor, p16Ink4a, and a tumor suppressor, p19Arf, is a pivotal target of Bmi1. Therefore, it would be of importance to understand the contribution of the Ink4a/Arf locus to Bmi1 oncogenic functions in cancer and search for as-yet-unknown Bmi1 target genes other than Ink4a/Arf. We used microarrays to explore novel candidate downstream targets for Bmi1 in hepatic stem/progenitor cells

2009-08-01 | GSE17462 | GEO

Transcription profiling of mouse Bmi1-overexpressing Ink4a-Arf-null hepatoblasts

2009-08-07 | E-GEOD-17462 | biostudies-arrayexpress

Transcription profiling of mouse neural stem cells derived from Ink4a/Arf-/- vs Bmi1-/-;Ink4a/Arf-/- mutants

Project description:Comparison of gene expression of Ink4a/Arf-/- vs Bmi1-/-;Ink4a/Arf-/- subventricular zone (SVZ) derived mouse neural stem cells (NSC) on Laminin (LM) and Fibronectin (FN) substrates.

2009-02-25 | E-NCMF-22 | biostudies-arrayexpress

Bmi1 mutant vs. WT dental epithelia

Project description:Transcriptional profiling of Bmi1 mutant dental epithelia including the stem cell compartment to determine which genes are upregulated in response to loss of Bmi1. Two condition experiment: dental epithelia homozygous null for Bmi1 and WT dental epithelia. 4 replicates each

2013-04-12 | E-GEOD-45999 | biostudies-arrayexpress

Transcription profiling of pre-injected brain cells from female INK4a/ARF knock-out, BMI1 INK4a/ARF knock-out mice and tumor cells derived from these mice

Project description:Comparison of gene expression profiles between pre-injected brain cells from female INK4a/ARF knock-out, BMI1 INK4a/ARF knock-out mice and tumor cells derived thereof.

2007-11-15 | E-NCMF-4 | biostudies-arrayexpress

Bmi1 functions as an oncogene independent of Ink4A/Arf repression in hepatic carcinogenesis.

Project description:Bmi1 is a polycomb group proto-oncogene that has been implicated in multiple tumor types. However, its role in hepatocellular carcinoma (HCC) development has not been well studied. In this article, we report that Bmi1 is overexpressed in human HCC samples. When Bmi1 expression is knocked down in human HCC cell lines, it significantly inhibits cell proliferation and perturbs cell cycle regulation. To investigate the role of Bmi1 in promoting liver cancer development in vivo, we stably expressed Bmi1 and/or an activated form of Ras (RasV12) in mouse liver. We found that while Bmi1 or RasV12 alone is not sufficient to promote liver cancer development, coexpression of Bmi1 and RasV12 promotes HCC formation in mice. Tumors induced by Bmi1/RasV12 resemble human HCC by deregulation of genes involved in cell proliferation, apoptosis, and angiogenesis. Intriguingly, we found no evidence that Bmi1 regulates Ink4A/Arf expression in both in vitro and in vivo systems of liver tumor development. In summary, our study shows that Bmi1 can cooperate with other oncogenic signals to promote hepatic carcinogenesis in vivo. Yet Bmi1 functions independent of Ink4A/Arf repression in liver cancer development.

| S-EPMC2796287 | biostudies-literature

Transcriptional coactivator Cited2 induces Bmi1 and Mel18 and controls fibroblast proliferation via Ink4a/ARF.

Project description:Cited2 (CBP/p300 interacting transactivator with ED-rich tail 2) is required for embryonic development, coactivation of transcription factor AP-2, and inhibition of hypoxia-inducible factor 1 transactivation. Cited2 is induced by multiple growth factors and cytokines and oncogenically transforms cells. Here, we show that the proliferation of Cited2(-/-) mouse embryonic fibroblasts ceases prematurely. This is associated with a reduction in growth fraction, senescent cellular morphology, and increased expression of the cell proliferation inhibitors p16(INK4a), p19(ARF), and p15(INK4b). Deletion of INK4a/ARF (encoding p16(INK4a) and p19(ARF)) completely rescued the defective proliferation of Cited2(-/-) fibroblasts. However, the deletion of INK4a/ARF did not rescue the embryonic malformations observed in Cited2(-/-) mice, indicating that INK4a/ARF-independent pathways are likely to be involved here. We found that Cited2(-/-) fibroblasts had reduced expression of the polycomb-group genes Bmi1 and Mel18, which function as INK4a/ARF and Hox repressors. Complementation with CITED2-expressing retrovirus enhanced proliferation, induced Bmi1/Mel18 expression, and decreased INK4a/ARF expression. Bmi1- and Mel18-expressing retroviruses enhanced the proliferation of Cited2(-/-) fibroblasts, indicating that they function downstream of Cited2. Our results provide genetic evidence that Cited2 controls the expression of INK4a/ARF and fibroblast proliferation, at least in part via the polycomb-group genes Bmi1 and Mel18.

| S-EPMC207593 | biostudies-literature

Elucidation of BMI1, RYBP and H2AK119ub interactomes in Glioblastoma

Project description:Identification of BMI1, RYBP and H2AK119UB interactome in Glioblastoma (GBM) to elucidate BMI1 roles independent of the PRC1-complex in GBM.

2021-09-09 | PXD022057 | Pride

BMI1 represses Ink4a/Arf and Hox genes to regulate stem cells in the rodent incisor.

Project description:The polycomb group gene Bmi1 is required for maintenance of adult stem cells in many organs. Inactivation of Bmi1 leads to impaired stem cell self-renewal due to deregulated gene expression. One critical target of BMI1 is Ink4a/Arf, which encodes the cell-cycle inhibitors p16(Ink4a) and p19(Arf). However, deletion of Ink4a/Arf only partially rescues Bmi1-null phenotypes, indicating that other important targets of BMI1 exist. Here, using the continuously growing mouse incisor as a model system, we report that Bmi1 is expressed by incisor stem cells and that deletion of Bmi1 resulted in fewer stem cells, perturbed gene expression and defective enamel production. Transcriptional profiling revealed that Hox expression is normally repressed by BMI1 in the adult, and functional assays demonstrated that BMI1-mediated repression of Hox genes preserves the undifferentiated state of stem cells. As Hox gene upregulation has also been reported in other systems when Bmi1 is inactivated, our findings point to a general mechanism whereby BMI1-mediated repression of Hox genes is required for the maintenance of adult stem cells and for prevention of inappropriate differentiation.

| S-EPMC3735916 | biostudies-literature

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