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Mll3 suppresses tumorigenesis by activating the Ink4a/Arf locus

ABSTRACT: Mll3 suppresses tumorigenesis by activating the Ink4a/Arf locus

PROVIDER: PRJNA336025 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3992260_1.fastq.gz	Fastqsanger.gz
	SRR3992260_2.fastq.gz	Fastqsanger.gz
	SRR3992280.fastq.gz	Fastqsanger.gz
	SRR3992290.fastq.gz	Fastqsanger.gz
	SRR3992261_1.fastq.gz	Fastqsanger.gz

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Mll3 suppresses tumorigenesis by activating the Ink4a/Arf locus [ChIP-seq]

Project description:Mutations in genes encoding epigenetic regulators are among the most frequent somatic events in human cancers. For example, missense and truncating mutations in the MLL3 (KTM2C) histone H3K4-methyltransferase gene can be found in several tumor types. MLL3 is a member of the mixed lineage leukemia gene family and component of the mammalian COMPASS/like complex that promotes gene expression by establishing chromatin modifications favoring gene activation. While Mll3 loss of function promotes tumorigenesis in mice, the molecular targets and biological processes underlying its anti-neoplastic effects remain unknown. Here we combine powerful genetic, genomic, and animal modeling approaches to demonstrate that Mll3 suppresses hepatocellular carcinoma (HCC) by promoting activation of the Cdkn2a (Ink4a/Arf) locus. Hence, disruption of Mll3 using CRISPR/Cas9-mediated genome editing or by RNA interference using short hairpin RNAs cooperates with the Myc oncogene to drive tumorigenesis, producing tumors with reduced H3K4 methylation at multiple gene regulatory elements and low levels of p16Ink4a and p19Arf expression. These results place MLL3 in an established tumor suppressor network and reveal how disruption of a conserved mechanism of epigenetic regulation can alter CDKN2A action and cancer development.

2017-08-01 | GSE85053 | GEO

Mll3 suppresses tumorigenesis by activating the Ink4a/Arf locus [RNA-seq]

2017-08-01 | GSE85049 | GEO

Mll3 suppresses tumorigenesis by activating the Ink4a/Arf locus

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-08-01 | GSE85055 | GEO

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

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

An inter-dependent network of enhancers regulates INK4a/ARF locus

Project description:By functionally dissecting densest enhancer cluster in the gene desert at 9P21 locus, we identified a non-redundant inter-dependent enhancer network that functions over long distances, the perturbation in any enhancer in the network results in the complete collapse of entire enhancer cluster and target genes activity. The enhancer network can be targeted to regulate INK4a/ARF locus in associated pathophysiologies and cancers.

2021-04-19 | GSE153410 | GEO

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

shGFP- and shQk-transduced Ink4a/Arf-/- Pten-/- primary mouse astrocytes

Project description:Identify potential QK-regulated mRNAs and linked pathways by comparing the transcriptional profiles of shGFP- and shQK-transduced Ink4a/Arf-/- Pten-/- primary mouse astrocytes Ink4a/Arf-/- Pten-/- primary mouse astrocytes infected with shQk-1, shQk-2 and infected with shGFP as control

2009-12-30 | E-GEOD-19687 | biostudies-arrayexpress

microRNA expression of Ink4a/Arf-/- Pten-/- mouse astrocytes

Project description:To identify QK-modulated microRNAs exhibiting a >1.5-fold change across all three cell model systems: human GBM cell lines, U87 and Hs683, and Ink4a/Arf-/- Pten-/- mouse astrocytes

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The Ink4a/Arf locus operates as a regulator of the circadian clock modulating RAS activity

Project description:Upon perturbations by RAS and by shBMAL, differential effects on the circadian phenotype were observed in wild type and Ink4a/Arf knockout MEFs which could be reproduced by modelling simulations and correlated with opposing cell cycle fate decisions.

2017-12-08 | E-MTAB-5943 | biostudies-arrayexpress

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