Similar Datasets
Project description:MN1 colocalizes with the BAF complex on enhancer chromatin
| PRJNA646758 | ENA
Project description:RNA-seq of murine HSPCs overexpressing MN1 or MN1-∆pQ
| PRJNA648119 | ENA
Project description:MN1 leukemia is a poor prognosis leukemia occuring as MN1 overexpression or fusion with TEL (MN1-TEL), MN1 and MN1-TEL show different biology in terms of dependence of known self-renewal associated genes in leukemia, c-kit positive murine primary bone marrow cells were retrovirally transduced with MN1, MN1-TEL or MN1-TEL mutant MN1-TELdelDBD showing biological similarity with MN1, after retroviral transformation of cells and 10 d culture RNA was extracted and gene expression profiling was assessed
2016-08-12 | GSE50877 | GEO
Project description:Expression of meningioma 1 (MN1) has been proposed to be a negative prognostic molecular marker in adult AML with normal cytogenetics, however its role in pediatric leukemia is unknown. We found elevated MN1 expression in 53 of 88 pediatric leukemia cases: significant amounts of MN1 were found in immature B-cell ALL and most cases of infant leukemia but no MN1 expression was detected in T-cell acute lymphoblastic leukemia (T-ALL). Interestingly 17 of 19 cases harboring MLL-X fusions showed also elevated MN1 expression. Lentiviral siRNA mediated MN1 knock-down resulted in cell cycle arrest and impaired clonogenic growth of 3 MLL-X-positive human leukemia cell lines overexpressing MN1 (THP-1, RS4;11, MOLM13). In a mouse MLL/ENL-induced leukemia MN1 overexpression resulted from retroviral provirus insertion. Strikingly co-expression of MN1 with MLL/ENL resulted in significantly reduced latency for induction of an AML phenotype in mice suggesting functional cooperation. MN1 overexpression in MLL/ENL-carrying cells resulted in expansion of the L-GMP population and facilitated disease induction in secondary recipients. Gene expression profiling allowed to define a number of potential MN1 hematopoietic targets. Up-regulation of CD34, FLT3, HLF, or DLK1 was validated in bone marrow transiently overexpressing MN1, in MN1-induced mouse leukemias, as well as in some cases of pediatric leukemias overexpressing MN1. Taken together, our work suggests that MN1 overexpression is essential for growth of leukemic cells, and that MN1 can act as a cooperating oncogene with MLL-X fusion genes most probably through modification of a distinct gene expression program that leads to expansion of a leukemia initiating cell population.
2009-06-01 | GSE13189 | GEO
Project description:Expression of meningioma 1 (MN1) has been proposed to be a negative prognostic molecular marker in adult AML with normal cytogenetics, however its role in pediatric leukemia is unknown. We found elevated MN1 expression in 53 of 88 pediatric leukemia cases: significant amounts of MN1 were found in immature B-cell ALL and most cases of infant leukemia but no MN1 expression was detected in T-cell acute lymphoblastic leukemia (T-ALL). Interestingly 17 of 19 cases harboring MLL-X fusions showed also elevated MN1 expression. Lentiviral siRNA mediated MN1 knock-down resulted in cell cycle arrest and impaired clonogenic growth of 3 MLL-X-positive human leukemia cell lines overexpressing MN1 (THP-1, RS4;11, MOLM13). In a mouse MLL/ENL-induced leukemia MN1 overexpression resulted from retroviral provirus insertion. Strikingly co-expression of MN1 with MLL/ENL resulted in significantly reduced latency for induction of an AML phenotype in mice suggesting functional cooperation. MN1 overexpression in MLL/ENL-carrying cells resulted in expansion of the L-GMP population and facilitated disease induction in secondary recipients. Gene expression profiling allowed to define a number of potential MN1 hematopoietic targets. Up-regulation of CD34, FLT3, HLF, or DLK1 was validated in bone marrow transiently overexpressing MN1, in MN1-induced mouse leukemias, as well as in some cases of pediatric leukemias overexpressing MN1. Taken together, our work suggests that MN1 overexpression is essential for growth of leukemic cells, and that MN1 can act as a cooperating oncogene with MLL-X fusion genes most probably through modification of a distinct gene expression program that leads to expansion of a leukemia initiating cell population. In three independent experiments bone marrow cells were transduced with MSCV-MN1-IRES/YFP or empty vector. 72h after transduction EYFP-positive cells were FACS-sorted and RNA isolated by ion-exchange chromatography with RNAmini (Qiagen) according to the manufacturerâs protocol
2010-04-08 | E-GEOD-13189 | biostudies-arrayexpress
Project description:Transcriptional effects of MN1 polyQ-stretch deletion in murine HSPCs
2020-07-24 | GSE154997 | GEO
Project description:The molecular mechanism defining susceptibility of normal cells to oncogenic transformation may be a valuable therapeutic target. We characterized the cell of origin and its critical pathways in MN1 leukemias. Common myeloid (CMP), but not granulocyte-macrophage progenitors (CMP) could be transformed by constitutively overexpressed MN1. Complementation studies of CMP-signature genes in GMPs demonstrated that leukemogenicity of MN1 required the MEIS1/abdB-like HOX protein complex. Colocalization studies by ChIP-seq identified common chromatin targets of MN1 and MEIS1 that were associated with open chromatin and transcriptional activation. Transcriptional repression of MEIS1 target sites in established MN1 leukemias had antileukemic activity. As MN1 relies on but can not activate expression of MEIS1/abdB-like HOX proteins, transcriptional activity of these genes determines which cell is the cell of origin in MN1 leukemia.
2011-05-19 | GSE22923 | GEO
Project description:Expression profiling of U937 derived cell lines with induced expression of MN1or MN1-TEL in combination with all-trans retinoic acid (ATRA) Keywords: expression profiling Two similar experiments (A and B, biological duplicates) were performed. Hybridization includes dye swaps. See experimental_design.jpg (below) for detailed setup of the study. In short, different time points after induction of MN1 or MN1-TEL were compared to uninduced samples. The effects of all-trans retinoic acid (ATRA) were also investigated
2008-09-09 | E-GEOD-11441 | biostudies-arrayexpress
Project description:To study the function of anti-MN1 sdAb in MN1-positive tumour cells, we treated U2OS cells with anti-MN1 sdAb and performed RNA-seq.
2022-10-30 | GSE214561 | GEO
Project description:Purpose: To characterize transcriptional changes associated with homozygous inactivation of Men1 in MN1 driven AML Methods: In vivo MN1 transformed cells were transduced with Cre-vector to inactivate Men1 and injected into sublethially irradiated syngeneic recipients. Men1-/- and Men1wt MN1-driven leukemic cells were isolated from moribund recipients and plated in methylcellulose for 7 days before RNA was extracted. Results: Men1-/- MN1-driven leukemic cells failed to propagate leukemia in most secondary recipients, in comparison with Men1wt MN1-driven. In vitro, cells had lost their colony forming activity. Gene expression analysis revealed a downregulation of the MN1 leukemic expression program. Conclusions: Men1 regulates long term maintenance of MN1-driven leukemia.
2020-05-09 | GSE150151 | GEO