Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA336033 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3992280.fastq.gz | Fastqsanger.gz | |||
| SRR3992290.fastq.gz | Fastqsanger.gz | |||
| SRR3992271.fastq.gz | Fastqsanger.gz | |||
| SRR3992281.fastq.gz | Fastqsanger.gz | |||
| SRR3992291.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 22 |
Similar Datasets
Project description:Mll3 suppresses tumorigenesis by activating the Ink4a/Arf locus [RNA-seq]
| PRJNA336036 | ENA
Project description:Mll3 suppresses tumorigenesis by activating the Ink4a/Arf locus
| PRJNA336025 | ENA
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
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 | GSE85049 | GEO
Project description:The Ink4a/Arf tumor supressors play crucial roles in inhibiting cell cycle progression at the G1/S checkpoint. Activating mutations in the KrasG12D oncogene is one of the most frequent changes in human cancer, with resultant constitutive mitogenic signaling within the cell. We generated cohorts of CD19Cre; KrasG12D/+; Ink4a/ArfL/+ mice to evaluate the combined contributions of Ink/Arf loss and KrasG12D activation in pre-B ALL lymphomas. In this data set we include the expression data obtained from pre-B ALL lymphomas isolated from mice with simultaneous deletion of the Ink/Arf locus and activation of KrasG12D oncogene (and CD19Cre; KrasG12D/+; Ink4a/ArfL/+ mice).
2015-05-30 | GSE69368 | GEO
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
Project description:Bmi1 is a component of polycomb repressive complex 1 and its role in the inheritance of the stemness of adult somatic stem cells has been well characterized. Bmi1 maintains the self-renewal capacity of adult stem cells, at least partially, by repressing the Ink4a/Arf locus that encodes a cyclin-dependent kinase inhibitor, p16Ink4a, and a tumor suppressor, p19Arf 14. Deletion of both Ink4a and Arf in Bmi1-deficient mice substantially restored the defective self-renewal capacity of HSCs and neural stem cells. Purified KSL cells from BM of wild-type, Bmi1-/-, Ink4a-/-Arf-/-, and Bmi1-/- Ink4a-/-Arf-/- mice were subjected to RNA extraction and hybridization on Affymetrix microarrays.
2011-02-21 | E-GEOD-19796 | biostudies-arrayexpress
Project description:microRNA expression of Ink4a/Arf-/- Pten-/- mouse astrocytes
| PRJNA124003 | ENA
Project description:Bmi1 is a component of polycomb repressive complex 1 and its role in the inheritance of the stemness of adult somatic stem cells has been well characterized. Bmi1 maintains the self-renewal capacity of adult stem cells, at least partially, by repressing the Ink4a/Arf locus that encodes a cyclin-dependent kinase inhibitor, p16Ink4a, and a tumor suppressor, p19Arf 14. Deletion of both Ink4a and Arf in Bmi1-deficient mice substantially restored the defective self-renewal capacity of HSCs and neural stem cells. Purified CMP from BM of recipient mice repopulated with wild-type, Ink4a-/-Arf-/-, and Bmi1-/- Ink4a-/-Arf-/- BM cells were subjected to RNA extraction and hybridization on Affymetrix microarrays.
2012-02-08 | E-GEOD-31086 | biostudies-arrayexpress
Project description:Inherited mutation in LKB1 results in the Peutz-Jeghers syndrome (PJS), characterized by intestinal hamartomas and a modestly increased frequency of gastrointestinal and breast cancer1. Somatic inactivation of LKB1 occurs in human lung adenocarcinoma2-4, but its tumor suppressor role in this tissue is unknown. Here we show that somatic Lkb1 deficiency strongly cooperates with somatic K-rasG12D activating mutation to accelerate the development of mouse lung tumorigenesis. Lkb1 deficiency in the setting of K-rasG12D mutation (K-ras Lkb1L/L) was associated with decreased tumor latency and increased tumor aggressiveness including metastasis. Furthermore, tumors from K-ras Lkb1L/L mice demonstrated histologies--squamous, adenosquamous and large cell--not seen with K-rasG12D mutation, Ink4a/Arf inactivation, or p53 inactivation alone or in combination. Experiments in vitro suggest that LKB1 suppresses lung tumorigenesis and progression through both p16INK4a-ARF-p53 dependent and independent mechanisms. These data indicate that LKB1 regulates lung tumor progression and differentiation. Keywords: cancer research
2007-08-28 | GSE6135 | GEO