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Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis [RNA-seq]

ABSTRACT: In this study, through a patient-sample driven transcriptomic and epigenetic description of the MF microenvironment landscape and cell-based analyses, we identify HOXB7 overexpression and more precisely a novel TGF-B-Wnt-HOXB7 pathway as associated to a pro-fibrotic and pro-osteoblastic biased differentiation of mesenchymal stromal cells (MSCs).

ORGANISM(S): Homo sapiens

PROVIDER: GSE234388 | GEO | 2024/12/18

REPOSITORIES: GEO

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Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis [ATAC-seq]

Project description:In this study, through a patient-sample driven transcriptomic and epigenetic description of the MF microenvironment landscape and cell-based analyses, we identify HOXB7 overexpression and more precisely a novel TGF-B-Wnt-HOXB7 pathway as associated to a pro-fibrotic and pro-osteoblastic biased differentiation of mesenchymal stromal cells (MSCs).

2024-12-18 | GSE234389 | GEO

Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis

Project description:Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis

| PRJNA981171 | ENA

Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-12-18 | GSE234390 | GEO

Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis [ATAC-seq]

Project description:Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis [ATAC-seq]

| PRJNA981175 | ENA

Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis [RNA-seq]

Project description:Comprehensive analysis of mesenchymal cells reveals a deregulated TGF-B/Wnt/HOXB7 axis in patients with myelofibrosis [RNA-seq]

| PRJNA981172 | ENA

Comprehensive analysis of mesenchymal cells reveals a dysregulated TGF-β/WNT/HOXB7 axis in patients with myelofibrosis.

Project description: Not available

| S-EPMC11623938 | biostudies-literature

Identification of mRNAs modulated by the HOXB7-MEK signaling cascade

Project description:Transcripts upregulated or downregulated by HOXB7-MEK signaling were identified for use on the microarray using the Affymetrix GeneChip WT PLUS Reagent Kit in comparison with HOXB7-knockdown S2-013 cells that were transfected with rescue-HOXB7 plasmid and treated with MEK inhibitor, and HOXB7-knockdown S2-013 cells that were transfected with rescue-HOXB7 plasmid but not treated with MEK inhibitor.

2017-09-13 | GSE97969 | GEO

human HCC cell MHCCLM3: HOXB7-siRNA transfected vs. control

Project description:We found that HOXB7 promotes HCC cell proliferation, migration, and invasion. To further explore the mechanism, we performed a cDNA microarray assay to compare the differential gene expression profiles of HOXB7 depletion (HOXB7-siRNA-treated) and negative control siRNA-treated in MHCCLM3 cells.

2019-04-02 | GSE80104 | GEO

Clinical drug response and proteotype profiling elucidates targetable vulnerabilities of myelofibrosis

Project description:Myelofibrosis (MF) is a hematopoietic stem cell disorder belonging to the myeloproliferative neoplasms. MF patients frequently carry driver mutations in JAK2 and Calreticulin (CALR) and have limited therapeutic options. Here, we integrate ex vivo drug response and proteotype analyses across MF patient cohorts to discover targetable vulnerabilities and associated therapeutic strategies. Drug sensitivities of mutated and progenitor cells were measured in patient blood using high-content imaging and single-cell deep learning-based analyses. Integration with matched molecular profiling revealed three therapeutic vulnerabilities. First, CALR mutations drive BET and HDAC inhibitor sensitivity, particularly in the absence of high MAPK-Ras pathway protein levels. Second, an MCM complex-high proliferative signature corresponds to advanced disease and sensitivity to drugs targeting pro-survival signaling and DNA replication. Third, homozygous CALR mutations result in high ER stress, responding to ER stressors and UPR inhibition. Overall, our integrated analyses provide a molecularly-motivated roadmap for individualized MF patient treatment.

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Identification of several potential chromatin binding sites of HOXB7 and its downstream target genes in breast cancer

Project description:We report the chromatin binding sites of HOXB7 transcription factor in BT-474 breast cancer cell line using ChIP-sequencing. We validated the chromatin binding sites in BT-474, MDA-MB-361, MCF7 and T-47D breast cancer cell lines using ChIP-qPCR. The ChIP experiments have been performed using HOXB7 antibody and IgG non-specific antibody as a negative control. The direct downstream target genes of HOXB7 were identified by analyzing the expression of genes located nearby HOXB7 binding sites in HOXB7 knockdown versus control cells using qRT-PCR.

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