HOXA13 Chromatin Immunoprecipitation on human HG18 Nimblegen 2 array promoter set
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE9922 | GEO | 2007/12/28
SECONDARY ACCESSION(S): PRJNA103921
REPOSITORIES: GEO
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Project description:HOXA13 Binding sites were located genome wide in primary human foreskin fibroblasts Tiled promoters with a probe per 100bp of refseq known genes 3kb upstream and 700 bp downstream of transcriptional start
2010-05-27 | E-GEOD-9922 | biostudies-arrayexpress
Project description:UTX binding sites were located genome wide in primary human fibroblasts (foot and lung) Tiled promoters with a probe per 100bp of refseq known genes 3kb upstream and 700 bp downstream of transcriptional start
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Project description:UTX binding sites were located genome wide in primary human fibroblasts (foot and lung) Tiled promoters with a probe per 100bp of refseq known genes 3kb upstream and 700 bp downstream of transcriptional start 8 samples (2 cell types (foot and lung primary human fibroblasts) x 2 set promoter arrays x 2 channels (channel 1 = ChIP = Cy5, channel 2 = input (10% of total genomic DNA hybed) = Cy3)
2010-06-24 | E-GEOD-16221 | biostudies-arrayexpress
Project description:HOXA13 was depleted by siRNA mediated technology in Foreskin Fibroblast at 20nM and 100nM siRNA concentration. As a control siGFP was used at 20nM and 100nM for respective gene expression comparisons.
2008-03-07 | E-SMDB-4279 | biostudies-arrayexpress
Project description:The goal of the experiment was to determine HOXA13 binding loci in human melanoma cells to infer downstream targets of a HOXA13 positional program.
2022-01-17 | GSE181768 | GEO
Project description:Background and aims: Class I Homeobox (HOX) genes are fundamental components of embryonic patterning and morphogenesis, also implicated in neoplastic transformations. Among them HOXA13, in particular, has been found to be the most overexpressed in HCC and to be associated with worse prognosis. However, no previous work has shown so far a direct causal effect between HOXA13 overexpression and liver tumorigenesis. In this study we aimed to prove the direct oncogenicity of HOXA13 in the liver and to unravel the molecular mechanisms of Hoxa13-induced liver tumorigenesis. Approach and Results: To unravel the oncogenic mechanism of HOXA13 in vivo, a transgenic mouse model of HOXA13 overexpression in the liver was generated using hydrodynamic tail vein injection coupled with a transposase system. The mice phenotype was followed over time, from 2 weeks up to 1-year post injection. RNA-sequencing was performed to monitor the transcriptomic changes over time. HOXA13-overexpression in the liver led to highly proliferative hepatocytes and correlated with the DNA damage marker yH2AX. 1-year post-injection 50% of the injected mice developed liver tumors of various histological grades and types. RNA-sequencing analysis performed on whole liver extracts of 2 weeks-old mice and tumors showed that the main pathway deregulated by HOXA13 overexpression was cell cycle, in particular G2/M transition and mitotic spindle assembly checkpoint. Additionally, HOXA13-overexpressing livers showed a transcriptomic signature of chromosomal Instability, suggesting a possible mechanism of tumorigenesis driven by genome instability. Conclusions: Our study highlights the role of HOXA13 as a novel oncogenic driver in hepatocarcinogenesis and strongly suggests that its oncogenic properties are least partially mediated by induction of chromosomal instability.
2021-02-09 | GSE166341 | GEO
Project description:Barrett’s esophagus in gastrointestinal reflux patients constitutes a columnar epithelium with distal characteristics, prone to progress to esophageal adenocarcinoma. HOX genes are known mediators of position-dependent morphology. Here we show HOX collinearity in the adult gut while Barrett’s esophagus shows high HOXA13 expression in stem cells and their progeny. HOXA13 overexpression appears sufficient to explain both the phenotype (through downregulation of the epidermal differentiation complex) and the oncogenic potential of Barrett’s esophagus. Intriguingly, employing a mouse model that contains a reporter coupled to the HOXA13 promotor we identify single HOXA13-positive cells distally from the physiological esophagus, which is mirrored in human physiology, but increased in BE. Additionally, we observe that HOXA13 expression confers a competitive advantage to cells. We thus propose that Barrett’s esophagus and associated esophageal adenocarcinoma is the consequence of expansion of this gastro-esophageal HOXA13-expressing compartment following epithelial injury.
2021-04-24 | GSE173169 | GEO
Project description:Barrett’s esophagus in gastrointestinal reflux patients constitutes a columnar epithelium with distal characteristics, prone to progress to esophageal adenocarcinoma. HOX genes are known mediators of position-dependent morphology. Here we show HOX collinearity in the adult gut while Barrett’s esophagus shows high HOXA13 expression in stem cells and their progeny. HOXA13 overexpression appears sufficient to explain both the phenotype (through downregulation of the epidermal differentiation complex) and the oncogenic potential of Barrett’s esophagus. Intriguingly, employing a mouse model that contains a reporter coupled to the HOXA13 promotor we identify single HOXA13-positive cells distally from the physiological esophagus, which is mirrored in human physiology, but increased in BE. Additionally, we observe that HOXA13 expression confers a competitive advantage to cells. We thus propose that Barrett’s esophagus and associated esophageal adenocarcinoma is the consequence of expansion of this gastro-esophageal HOXA13-expressing compartment following epithelial injury.
2021-04-24 | GSE173166 | GEO
Project description:Transcriptional profiling of mouse embryonic stem cells comparing control (dCas9 transfected) ES cells with ES cells transfected with a Hottip promoter gRNAs and Hoxa13 promoter gRNAs along with dCAs9-VP160. Goal was to determine the effects of activation of Hottip lncRNA and Hoxa13 on expression of Hox genes
2017-03-10 | GSE95064 | GEO
Project description:Barrett’s esophagus in gastrointestinal reflux patients constitutes a columnar epithelium with distal characteristics, prone to progress to esophageal adenocarcinoma. HOX genes are known mediators of position-dependent morphology. Here we show HOX collinearity in the adult gut while Barrett’s esophagus shows high HOXA13 expression in stem cells and their progeny. HOXA13 overexpression appears sufficient to explain both the phenotype (through downregulation of the epidermal differentiation complex) and the oncogenic potential of Barrett’s esophagus. Intriguingly, employing a mouse model that contains a reporter coupled to the HOXA13 promotor we identify single HOXA13-positive cells distally from the physiological esophagus, which is mirrored in human physiology, but increased in BE. Additionally, we observe that HOXA13 expression confers a competitive advantage to cells. We thus propose that Barrett’s esophagus and associated esophageal adenocarcinoma is the consequence of expansion of this gastro-esophageal HOXA13-expressing compartment following epithelial injury.
2021-04-24 | GSE173168 | GEO