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Prevention of mammary tumor progression by silencing HoxA1 via intraductal injection of nanoparticle-formulated siRNA

ABSTRACT: Silencing HoxA1 in vivo by intraductal delivery of nanoparticle-formulated siRNA reduced mammary tumor incidence by 75% , reduced cell proliferation, and prevented loss of ER and PR expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE50813 | GEO | 2013/12/31

SECONDARY ACCESSION(S): PRJNA219072

REPOSITORIES: GEO

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Prevention of mammary tumor progression by silencing HoxA1 via intraductal injection of nanoparticle-formulated siRNA

Project description:Silencing HoxA1 in vivo by intraductal delivery of nanoparticle-formulated siRNA reduced mammary tumor incidence by 75% , reduced cell proliferation, and prevented loss of ER and PR expression. 8 week wild type FVB mouse whole mammary gland and 8week to 20 week transgenic FVB C3(1)-SV40Tag mouse whole mammary gland

2013-12-31 | E-GEOD-50813 | biostudies-arrayexpress

Mus musculus

Project description:Prevention of mammary tumor progression by silencing HoxA1 via intraductal injection of nanoparticle-formulated siRNA

| PRJNA219072 | ENA

E-GEOD-50813

Project description:Prevention of mammary tumor progression by silencing HoxA1 via intraductal injection of nanoparticle-formulated siRNA

2015-07-27 | E-GEOD-50813 | ExpressionAtlas

Identification of Hoxa1 downstream targets

Project description:To better understand the role of Hoxa1 during embryogenesis and gain insight to the transcriptional network controlled by this gene, we carried out a large-scale screening for Hoxa1 downstream targets by performing microarray analysis. Tissue from the rhombomere 3-5 region of wildtype and Hoxa1 null embryos, including neuroectoderm, mesoderm and otic ectoderm was microdissected at the peak of Hoxa1 expression. RNA from wildtype and Hoxa1Δ/Δ samples was hybridized to the Agilent mouse whole genome array.

2011-09-03 | GSE25868 | GEO

Modeling myelodysplastic syndromes in mice by altered Hoxa1 spliceform expression

Project description:The homeobox gene, Hoxa1, has two different isoforms generated by alternative splicing: a full-length homeodomain-containing Hoxa1 (Hoxa1-FL), and a truncated Hoxa1 (Hoxa1-T), that lacks the homeodomain. Oncoretroviral overexpression of wildtype Hoxa1 cDNA (WT-Hoxa1), which generates both Hoxa1 isoforms, in murine hematopoietic stem and progenitor cells (HSPCs) perturbed hematopoiesis, resulting in myelodysplastic syndromes (MDS) in mice. Overexpression of a mutated Hoxa1 cDNA (MUT-Hoxa1) that generates Hoxa1-FL but not Hoxa1-T led to a more severe MDS capable of transforming to secondary acute myeloid leukemia (sAML). Similar to human MDS, DNA damage repair pathways were downregulated in Hoxa1-overexpressing hematopoietic progenitor cells. Conditional knock-in mouse models revealed a Hoxa1-FL dosage-dependent effect on MDS disease severity. Our data reveal that increased expression of Hoxa1-FL in HSPCs is sufficient to initiate MDS in mice. CD34+ cells from up to 50% of patients with MDS had elevated HOXA1-FL expression, highlighting the clinical relevance of our mouse models.

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Modeling myelodysplastic syndromes in mice by altered Hoxa1 spliceform expression (CMP)

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Hoxa1 LoF RNA-seq

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A distal enhancer maintaining Hoxa1 expression orchestrates retinoic acid-induced early ESCs differentiation

Project description:Retinoic acid (RA) induces rapid differentiation of ESCs, partly by activating expression of the transcription factor Hoxa1, which regulates downstream target genes that promote ESCs differentiation. However, mechanisms of RA-induced Hoxa1 expression and ESCs early differentiation remain largely unknown. Here, we identify a distal enhancer interacting with the Hoxa1 locus through a long-range chromatin loop. Enhancer deletion significantly inhibited expression of RA-induced Hoxa1 and endoderm master control genes such as Gata4 and Gata6. Transcriptome analysis revealed that RA-induced early ESCs differentiation was blocked in Hoxa1 enhancer knockout cells, suggesting a requirement for the enhancer. Restoration of Hoxa1 expression partly rescued expression levels of ~40% of genes whose expression changed following enhancer deletion, and ~18% of promoters of those rescued genes were directly bound by Hoxa1. Our data show that a distal enhancer maintains Hoxa1 expression through long-range chromatin loop and that Hoxa1 directly regulates downstream target gene expression and then orchestrates RA-induced early differentiation of ESCs.

2018-12-24 | GSE124306 | GEO

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