Expression data from HoxA9wt/Meis1 vs. HoxA9AA/Meis1 mouse models
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PROVIDER: PRJNA1219406 | ENA |
REPOSITORIES: ENA
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Project description:To verify the impact of eIF4E activation on HoxA9-induced leukemic transformation in vivo, we made a double point mutation (HoxA9AA) to disrupt the physical and functional interaction between eIF4E and HOXA9. Microarray analysis of transformed leukemic cell lines derived from HoxA9wt/Meis1 and HoxA9AA/Meis1 leukemic cells presented highly similar transcriptome profile, without any significant changes of HoxA9 gene signature.
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Project description:In order to identify direct gene targets and pathways regulated by MEIS1 in prostate cells and identify mechanisms of observed tumor suppression with MEIS1 expression, we performed Chromatin Immunoprecipitation and sequencing (ChIP-seq) of MEIS1 in the CWR22Rv1-LV-MEIS1 line. Also, given the dependence of HOXB13, and to enable determination of HOXB13-dependent vs. HOXB13-independent MEIS1 DNA binding, we performed parallel MEIS1 ChIP-seq in the CWR22Rv1-HOXB13ko-LV-MEIS1 line. LV-MEIS1 denotes cells with exogenous lentiviral expression of MEIS1, and they still express endogenous HOXB13. Knockout of HOXB13 was achieved by CRISPR and validated with western blotting. HOXB13ko-LV-MEIS1 denotes cells where the same lentiviral expression of MEIS1 was infected into the HOXB13ko cells, so these cells are positive for MEIS1 expression and negative for HOXB13.
2020-07-15 | GSE132716 | GEO
Project description:Meis1 is found cooperatively activated with Hoxa7/a9 in AML, and it indeed promotes leukemogenic activities of Hoxa9. It is important to identify downstream target genes of Meis1 to understand its cooperative activity with Hoxa9 in leukemogenesis. We used microarrays to detail the global programme of gene expression upon Meis1 knockout. Murine primary bone marrow cells of the Rosa26-Cre-ERT2 knock-in mouse were transformed by retroviral transduction of Hoxa9 and floxed Meis1. The immortalized bone marrow cells were treated with 2 μM of 4-hydroxytamoxifen to delete Meis1 cDNA. Gene expression profiles were compared between the original Hoxa9/Meis1-expressing cells and Meis1 deleted (Hoxa9 only) cells.
2015-01-01 | E-GEOD-50645 | biostudies-arrayexpress
Project description:We conducted RNA-sequencing to determine MEIS1-mediated gene regulation in prostate cancer cells because phenotypic data has demonstrated that expression of MEIS1 is sufficient to slow tumor growth and metastatic colonization in vitro and in vivo. These analyses compared global gene expression of CWR22Rv1-Control and CWR22Rv1-LV-MEIS1, as well as the HOXB13ko and HOXB13ko-LV-MEIS1 cells to precisely delineate MEIS1 and HOXB13-regulated genes. Importantly, inclusion of HOXB13ko lines enabled determination of HOXB13-associated gene regulation, as well as identification of significant changes between LV-MEIS1 vs. Control that are HOXB13-independent and thus unrelated to tumor suppression. Are samples are from CWR-22Rv1 cells. Control denotes cells with constitutive expression of Cas9, but with no gRNA provided. Control cells have nearly undetectable levels of endogenous MEIS1 expression, but do express HOXB13. LV-MEIS1 denotes cells with exogenous lentiviral expression of MEIS1, and they still express endogenous HOXB13. HOXB13ko denotes cells where HOXB13 was knocked out using CRISPR, 6 cell clones were isolated with confirmed HOXB13 knockout by western blot and pooled together into one line, so these cells lack both MEIS1 and HOXB13. HOXB13ko-LV-MEIS1 denotes cells where the same lentiviral expression of MEIS1 was infected into the HOXB13ko cell pool, so these cells are positive for MEIS1 expression and negative for HOXB13.
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Project description:Meis1 is a transcription factor involved in a broad range of functions including development and proliferation and has been previously shown to harness cell cycle progression. This study aimed to investigate the regulation of Meis1 by long non-coding RNAs (lncRNAs) and their sponged microRNAs (miRNAs) and hence the impact of this regulatory axis on cell proliferation. Using in-silico analysis, miR-499-5p was predicted to target Meis1 and Malat1 was predicted and previously proven to sponge miR-499-5p. We showed that forcing the expression of miR-499-5p downregulates Meis1 expression in C166 cell line by directly binding to its 3’UTR. In addition, Malat1 knockdown significantly increases miR-499-5p expression, subsequently suppressing Meis1 mRNA and protein expression levels. Furthermore, the impact of manipulating the Malat1/miR-499-5p/Meis1 axis on cellular proliferation was assessed using the BrdU incorporation assay. We demonstrated that upon knockdown of Malat1, mimicking with miR-499-5p, or knockdown of Meis1, cell proliferation was induced. Gene Ontology, KEGG and Reactome enrichment analyses were performed on proteins detected by mass spectrometry following manipulation of the Malat1/miR-499-5p/Meis1 axis. The data revealed a multitude of differentially expressed proteins (DEPs) significantly enriched in processes related to cell cycle, cell division and proliferation. These DEPs were also involved in key signaling pathways, such as Wnt and mTOR, known to play critical roles in cell proliferation and cell cycle. Finally, since Malat1 and miR-499-5p are conserved in humans and mice, we examined the expression pattern of both non-coding RNAs (ncRNAs) in the hearts of neonatal, postnatal, and adult mice, representing models of proliferative and non-proliferative tissues. We demonstrated a paradoxical expression pattern, where Malat1 is underexpressed while miR-499-5p is overexpressed in proliferative neonatal cardiomyocytes. Collectively, our findings confirm that Malat1 sponges miR-499-5p which directly regulates Meis1, and that Malat1/miR-499-5p/Meis1 axis has a pivotal influence on cellular proliferation.
2025-05-07 | PXD054558 | Pride
Project description:Meis1 is found cooperatively activated with Hoxa7/a9 in AML, and it indeed promotes leukemogenic activities of Hoxa9. It is important to identify downstream target genes of Meis1 to understand its cooperative activity with Hoxa9 in leukemogenesis. We used microarrays to detail the global programme of gene expression upon Meis1 knockout.
2015-01-01 | GSE50645 | GEO
Project description:Meis1 encodes a TALE family homeodomain protein that was first identified as a common retroviral integration site in mouse BHX2 myeloid leukemia. It functions as a DNA binding co-factor of Hox proteins through interacting with Pbx, a member of another TALE family protein. Moreover, Meis1 homozygous knockout mice are embryonic lethal, showing significant defects in vasculogenesis, eye development and hematopoiesis. Severe defects were also observed in adult hematopoiesis by conditional inactivation of Meis1 in vivo. Meis1 is critical to maintain the balance between enter and exit from cell cycles of hematopoietic stem cells (HSCs), indicating that Meis1 regulates self-renewal and quiescence of HSCs.
2013-12-01 | GSE38336 | GEO
Project description:Analysis of thymic epithelial cells lacking Meis1 gene using K14-CreERT2 Meis1fl/fl mice. Meis1 is a TALE class homeodomain transcription factor that critically regulates numerous embryonic developmental processes. Results provide insight into the role of Meis1 in the maintenance of postnatal thymic epithelial cells. Meis1-regulated gene expression in CD45- EpCAM+ mouse thymic epithelial cells was measured at 4 days after the induction of Meis1 deletion. Two independent experiments (pools of 6 mice; 2 pools per genotype) were performed.
2012-11-30 | E-GEOD-30824 | biostudies-arrayexpress
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