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HOXA5 depletion in MCF10A cells

ABSTRACT: Microarray analysis of gene expression in MCF10A cells following HOXA5 depletion.

ORGANISM(S): Homo sapiens

PROVIDER: GSE75840 | GEO | 2016/02/01

SECONDARY ACCESSION(S): PRJNA305516

REPOSITORIES: GEO

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Homo sapiens

Project description:HOXA5 depletion in MCF10A cells

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The role HOXA5 in extrahepatic cholangiocarcinoma (Methylation)

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The role HOXA5 in extrahepatic cholangiocarcinoma (Expression)

Project description:Homeobox A5 (HOXA5) is a transcription factor in mammals and can regulate cell differentiation, proliferation and apoptosis as well as tumorigenesis. However, little is known about whether and how HOXA5 can regulate the malignant behaviors of cholangiocarcinoma. The expression profiles were analyzed by RNA microarray. We found MXD1 was upregulated upon HOXA5 overexpression. Besides, p53 pathway was activated by HOXA5 overexpression.

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HOXA5 transcriptional targets

Project description:HOXA5 inducible cell line Hs578T was established and cultured as described previously (MCB 2004. 24:924-935). 2×106 cells were seeded onto a 10-cm cell culture dish at 24h before induction. Two batches of RNA from HOXA5-inducible cells (0 h, 6 h and 9 h) were purified for repeating the microarray hybridization experiments once using Affymatrix Chips.Total RNA was extracted using TRIzol reagent (Gibco BRL, Life Technologies, Grand Island, NY) and purified using the RNeasy Mini Kit (Qiagen, Valencia, CA). Keywords: time-course

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Transcriptome analysis of MCF10A-M2 cells upon the depletion of OVOL1 or OVOL2

Project description:Transcriptome analysis of MCF10A-M2 cells upon the depletion of OVOL1 or OVOL2

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Loss of Hoxa5 function affects Hox gene expression in different biological contexts

Project description:Hoxa5 plays numerous roles in development, but its downstream molecular effects are mostly unknown. We applied bulk RNA_seq assays to characterize the transcriptional impact of the loss of Hoxa5 gene function in seven different biological contexts, including developing respiratory and musculoskeletal tissues that present phenotypes in Hoxa5 mouse mutants. This global analysis revealed few shared transcriptional changes, suggesting that HOXA5 acts mainly via the regulation of context_specific effectors. However, Hox genes themselves appeared as potentially conserved targets of HOXA5 across tissues. Notably, a trend toward reduced expression of HoxA genes was observed in Hoxa5 null mutants in several tissue contexts. Comparative analysis of epigenetic marks along the HoxA cluster in lung tissue from two different Hoxa5 mutant mouse lines revealed limited effect of either mutation indicating that Hoxa5 gene targeting did not significantly perturb the chromatin landscape of the surrounding HoxA cluster. Combined with the shared impact of the two Hoxa5 mutant alleles on phenotypes and Hox expression, these data argue against the contribution of local cis effects to Hoxa5 mutant phenotypes and support the notion that the HOXA5 protein acts in trans in the control of Hox gene expression.

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The binding pattern of HOXA5 in the genome of extrahepatic cholangiocarcinoma cells

Project description:HOXA5 is a transcription factor in mammalian and can regulate cell differentiation, proliferation and apoptosis as well as tumorigenesis. However, little is known on whether and how HOXA5 can regulate the malignant behaviors of cholangiocarcinoma. The binding pattern of HOXA5 was evaluated by CUT & Tag assay. The differential peaks were analysed to assess the role of HOXA5 in the regulation of the key genes involved in cell proliferation and DNA replication.

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Transcription profiling time series of HOXA5 induction in human Hs578T cell line

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HOXA5 counteracts stem cell traits by inhibiting Wnt signaling

Project description:Here we identify HOXA5 as an important repressor of intestinal stem cell fate in vivo and identify a reciprocal feedback between HOXA5 and Wnt signaling. HOXA5 is suppressed by the Wnt pathway to maintain stemness and becomes active only outside the intestinal crypt where it inhibits Wnt signaling to enforce differentiation. In colon cancer, HOXA5 is down-regulated and its re-expression induces loss of the cancer stem cell phenotype preventing tumor progression and metastasis. Tumor regression by HOXA5 induction can be triggered by retinoids, which represents a tangible means to treat colon cancer by eliminating cancer stem cells. We use microarrays to identify HOXA5 signature in SW480 human colon carcinoma cell line

2015-12-13 | GSE74862 | GEO

Identification of p53-regulated genes in breast epithelial cells using MCF10A with wild-type p53 or p53-null

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2017-05-10 | GSE98727 | GEO

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