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

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

PROVIDER: PRJNA1124161 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29422222_1.fastq.gz	Fastqsanger.gz
	SRR29422222_2.fastq.gz	Fastqsanger.gz
	SRR29422223_1.fastq.gz	Fastqsanger.gz
	SRR29422223_2.fastq.gz	Fastqsanger.gz
	SRR29422224_1.fastq.gz	Fastqsanger.gz

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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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Project description:Homeobox A5 (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 methylation levels of HOXA5 were evaluated by methylation microarray and bisulfite sequencing PCR. We found that hypermethylation in the HOXA5 promoter down-regulated HOXA5 expression in extrahepatic cholangiocarcinoma (ECCA) tissues, which was correlated with worse overall survival. HOXA5 over-expression significantly inhibited the proliferation and tumor growth.

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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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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

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Project description:Homeobox genes comprise a family of regulatory genes that contain a common homeobox domain and act as transcription factors. Changes in the expression of homeobox genes are observed in many cancers, including leukaemia, colon, skin, prostate, breast, and ovarian cancers. Recent studies indicate that homeobox A5 (HOXA5) may serve as a tumour suppressor gene in breast cells. However, the precise role of HOXA5 in lung cancer remains unclear. Using microarrays and an invasion/metastasis lung adenocarcinoma cell line model, we showed that the expression of HOXA5 is negatively correlated with cancer cell invasion ability. The ectopic expression of HOXA5 in highly invasive cancer cells suppressed cell migration, invasion, and filopodia formation in vitro and inhibited metastatic potential in vivo. The knockdown of HOXA5 expression via a HOXA5-specific siRNA was able to promote the invasiveness of lung cancer cells. Furthermore, HOXA5 expression was associated with improved overall survival and disease-free survival in non-small cell lung cancer patients with wild-type EGFR (P = 0.0199 and 0.0345, respectively). Genome-wide transcriptome and pathway analyses indicated that these effects of HOXA5 may be associated with the regulation of cytoskeletal remodelling. In summary, our studies provide new insights into how HOXA5 may contribute to the suppression of metastasis in lung cancer. We used microarrays to profile the global gene expression of HOXA5-overexpressing cells compared with mock control cells and identified the pathways involved in HOXA5-induced biofunctional alterations.

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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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