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LMO2 is critical for early metastatic events in breast cancer

ABSTRACT: LMO2 is critical for early metastatic events in breast cancer

PROVIDER: PRJNA668290 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12800248_1.fastq.gz	Fastqsanger.gz
	SRR12800248_2.fastq.gz	Fastqsanger.gz
	SRR12800249_1.fastq.gz	Fastqsanger.gz
	SRR12800249_2.fastq.gz	Fastqsanger.gz
	SRR12800250_1.fastq.gz	Fastqsanger.gz

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LMO2 is critical for early metastatic events in breast cancer

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

2023-10-08 | GSE159285 | GEO

Lmo2 is dispensable for maintenance of most Lmo2-induced murine T-cell leukemias

Project description:Lmo2 is an oncogenic transcription factor that is a frequent target of chromosomal abnormalities in this T-cell acute lymphoblastic leukemia (T-ALL). In transgenic mouse models, overexpression of Lmo2 causes thymocyte self-renewal leading to T-cell leukemia with long latency. However, the requirement of Lmo2 for maintenance of overt leukemia is poorly understood. We found that Lyl1, a critical cofactor for Lmo2-induced leukemia, is frequently lost in cell lines derived from Lmo2-transgenic mice, raising the possibility that Lmo2 function is dispensable at this stage. To study this, we developed a Tetracycline-repressible knock-in mouse model (Vav-TRE-Lmo2), which expresses Lmo2 throughout the haematopoietic system. This led to specific effects on T-cell development and the development of T-cell leukemia with long latency, preceded by the presence of self-renewing T-cells in the thymus. Repression of Lmo2 overcame the Lmo2-induced thymocyte developmental block at the preleukemic stage and led to elimination of Lmo2-induced thymocyte self-renewal in vivo. In contrast, Lmo2 function was dispensable for the majority of overt Lmo2-induced T-cell leukemias as well as leukemia-derived cell lines, implying an evolution of oncogene addiction in the majority of T-cell leukemias. Lmo2-dependence in T-ALL was associated with an immature gene expression profile, but could not be predicted by immunophenotype or assessment of Notch pathway activation. Thus, Lmo2 can give rise to both Lmo2-depenent and –independent T-cell leukemias. The Vav-TRE-Lmo2 model should be useful to determine the molecular features associated with Lmo2-dependence, as well as the critical components of the Lmo2-induced self-renewal pathways in T-ALL.

2022-01-01 | GSE125674 | GEO

Requirement for Lyl1 in a model of Lmo2-driven early T-cell precursor ALL

Project description:To determine the requirement for Lyl1 in Lmo2-driven T-ALL, microarray data was perepared from sorted CD4-CD8 double negative thymocytes of wild-type, Lmo2 transgenic and Lmo2-transgenic, Lyl1 knockout mice.

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Requirement for Lyl1 in a model of Lmo2-driven early T-cell precursor ALL

2013-07-25 | E-GEOD-49164 | biostudies-arrayexpress

Human LMO2 binding protein LC-MSMS in U87MG(Glioblastoma cell)

Project description:To identify the binding partner of LMO2 for explanation of STAT3 signal-related protein in human glioblastoma

2022-08-11 | PXD028254 | Pride

Ldb1 is required for Lmo2 oncogene-induced thymocyte self-renewal and T-cell Acute Lymphoblastic Leukemia

Project description:Prolonged or enhanced expression of the proto-oncogene Lmo2 is associated with a severe form of T-cell Acute Lymphoblastic Leukemia (T-ALL), designated Early T-progenitor ALL (ETP-ALL), that is characterized by the aberrant self-renewal and subsequent oncogenic transformation of immature thymocytes. Recent data suggest that Lmo2 may exert these effects by functioning as component of a multi-subunit transcription complex that includes the ubiquitous adapter Ldb1 along with b-HLH and/or GATA family transcription factors. In this study, we investigated the importance of Ldb1 for Lmo2-induced T-ALL by conditional deletion of Ldb1 in thymocytes in a Lmo2 transgenic mouse model of T-ALL. Our results identify a critical requirement for Ldb1 in the induction of thymocyte self-renewal, thymocyte radio-resistance and transition to T-ALL in Lmo2 transgenic mice. Ldb1 was also required for acquisition of the pre-leukemic ETP gene expression signature in immature Lmo2 transgenic thymocytes. Together, these results support a model where Lmo2-induced T-ALL results from failure to down-regulate Ldb/Lmo2 nucleated transcription complexes that normally function to enforce self-renewal in bone marrow hematopoietic progenitors

2020-03-19 | GSE129244 | GEO

caArray_carpt-00469: Copy Number and Targeted Mutational Analysis Reveals Novel Somatic Events in Metastatic Prostate Tumors

Project description:A comprehensive genomic survey for somatic events in systemic metastatic prostate tumors.

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Identification of LMO2 transcriptome and interactome in diffuse large B-cell lymphoma

Project description:LMO2 regulates gene expression facilitating the formation of multipartite DNA-binding complexes. In B cells, LMO2 is specifically up-regulated in the Germinal Center (GC) reaction and is expressed in GC-derived non-Hodgkin’s lymphomas. LMO2 is one of the most powerful prognostic indicators in DLBCL patients. However, its function in GC B cells and DLBCL is currently unknown. In the present study we characterized the LMO2 transcriptome and interactome in DLBCL cells. LMO2 regulates genes implicated in kinetochore function, chromosome assembly and mitosis. Overexpression of LMO2 in DLBCL cell lines results in centrosome amplification. In DLBCL, the LMO2 complex contains some of the traditional partners such as LDB1, E2A, HEB, Lyl1, ETO2 and SP1, but not TAL1 or GATA proteins. Furthermore, we identified novel LMO2 interacting partners: ELK1, NFATc1 and LEF-1 proteins. Reporter assays revealed that LMO2 increases transcriptional activity of NFATc1 and decreases transcriptional activity of LEF-1 proteins. Overall, our studies identified a novel LMO2 transcriptome and interactome in DLBCL and provide a platform for future elucidation of LMO2 function in GC B-cells and DLBCL pathogenesis.

2012-07-13 | GSE34576 | GEO

Identification of LMO2 transcriptome and interactome in diffuse large B-cell lymphoma

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Expression analysis of breast cancer cell lines SKBR-3 and ZR-75-1 upon treatment of LMO2 overexpression or knocking-down

Project description:Investigation of whole genome gene expression level changes in ZR-75-1 cells with knocking-down of LMO2, and in SKBR-3 cells with overexpression of LMO2, compared to their relative control cells.

2017-11-18 | GSE105020 | GEO

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