Potential mechanisms of HOXA5 in AML by RNA-seq analysis
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE304381 | GEO | 2026/08/31
REPOSITORIES: GEO
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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:Despite the fundamental role of Hoxa5 in mouse development revealed by the well-characterized phenotypes of Hoxa5 mutant mice, HOXA5-dependent regulatory networks remain ill-defined. We generated a Hoxa5FLAG epitope-tagged mouse line to perform ChIP-seq experiments and uncover genome-wide occupancy of the HOXA5 protein. This was done in the developing lung tissue, in which Hoxa5 plays a predominant role since Hoxa5-/- mouse mutants die at birth from respiratory defects. ChIP-seq allowed us to define an in vivo HOXA5 binding motif and its widespread genome distribution in the embryonic lung. Combined with ATAC-seq assays and epigenetic analyses, HOXA5 targets were identified. They include Hox genes known to show expression changes in lungs from Hoxa5 null mutant embryos. Moreover, several key actors of lung morphogenesis were found to possess HOXA5-binding sites and appeared as potential targets of HOXA5. Impact of the loss of Hoxa5 function on their expression was confirmed by in situ hybridization. These targets include members of the FGF10, SHH, BMP4 and WNT2 signaling pathways. Altogether, these data unveil the crucial role of HOXA5 in the coordinated control of the signaling networks instructing lung development.
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Project description:Despite the fundamental role of Hoxa5 in mouse development revealed by the well-characterized phenotypes of Hoxa5 mutant mice, HOXA5-dependent regulatory networks remain ill-defined. We generated a Hoxa5FLAG epitope-tagged mouse line to perform ChIP-seq experiments and uncover genome-wide occupancy of the HOXA5 protein. This was done in the developing lung tissue, in which Hoxa5 plays a predominant role since Hoxa5-/- mouse mutants die at birth from respiratory defects. ChIP-seq allowed us to define an in vivo HOXA5 binding motif and its widespread genome distribution in the embryonic lung. Combined with ATAC-seq assays and epigenetic analyses, HOXA5 targets were identified. They include Hox genes known to show expression changes in lungs from Hoxa5 null mutant embryos. Moreover, several key actors of lung morphogenesis were found to possess HOXA5-binding sites and appeared as potential targets of HOXA5. Impact of the loss of Hoxa5 function on their expression was confirmed by in situ hybridization. These targets include members of the FGF10, SHH, BMP4 and WNT2 signaling pathways. Altogether, these data unveil the crucial role of HOXA5 in the coordinated control of the signaling networks instructing lung development.
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Project description:Purpose：We used transcriptome sequencing to study the mechanism of sugar and lipid excesses on nematode growth and development. Methods：Nematodes grew to L4 phase and collected nematodes from different treatment groups, including control group without any treatment, 400 mM sucrose, 500 ug/ml stearic acid, co-treatment with sucrose and stearic acid, and co-treatment with resveratrol-sucrose-stearic acid, 3 replicates per group. Extract total RNA, detect RNA quality, library preparation, sequencing, and analyze data Results:Reads were obtained for each sample using Illumina Hiseq X Ten sequencing. After discarding the low-quality reads, corresponding to 48 million clean reads obtained from sequencing were mapped on the reference genome of C. elegans (GCF_000002985.6). High Pearson's correlation coefficients of FPKM distribution between the three biological replicates for each sample were detected (R2 = 0.93-0.99, P < 0.001) , reflecting the robustness of our library preparation from nematodes’ RNA samples.Compared with control group, there were 905 DEGs in the sucrose group , of which 387 genes were upregulated and 518 genes were downregulated. Similarly, there were 698 DEGs in the stearic acid group , including 367 upregulated and 331 downregulated DEGs. Compared with control group, there were 1014 DEGs in group SUC-STE, including 476 upregulated DEGs, and 538 downregulated DEGs. Moreover, in contrast to the sucrose-stearic acid group, there were 10 DEGs after treated with resveratrol, including 5 upregulated DEGs and 5 downregulated DEGs.
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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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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 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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