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The co-receptor Neuropilin-1 enhances proliferation in inv(16) acute myeloid leukemia via VEGF signaling

ABSTRACT: The co-receptor Neuropilin-1 enhances proliferation in inv(16) acute myeloid leukemia via VEGF signaling

PROVIDER: PRJNA890312 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21898875.fastq.gz	Fastqsanger.gz
	SRR21898876.fastq.gz	Fastqsanger.gz
	SRR21898877.fastq.gz	Fastqsanger.gz
	SRR21898878.fastq.gz	Fastqsanger.gz
	SRR21898879.fastq.gz	Fastqsanger.gz

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The co-receptor Neuropilin-1 enhances proliferation in inv(16) acute myeloid leukemia via VEGF signaling

Project description:Oncogenic programs regulate the proliferation and maintenance of cancer stem cells, and can define pharmacologic dependencies. In acute myeloid leukemia (AML) with the chromosome inversion 16 (inv(16)), the fusion CBF::MYH11 oncoprotein regulates pathways associated with leukemia stem cell activity. Here we demonstrate that expression of Neuropilin-1 (NRP1) is regulated by the fusion oncoprotein, and promotes AML expansion. Mechanistically, we show that the NRP1 locus has open chromatin in inv(16) AML, and that CBF::MYH11 modulates the local function of the transcription factors ERG, GATA2 and RUNX1 to sustain NRP1 levels. We found that ERG activates NRP1 expression, and that CBF::MYH11 knockdown represses ERG expression, thereby allowing the repressive activity of GATA2/RUNX1 at three NRP1 enhancers. Functionally, we demonstrate that NRP1 enhances the expansion of leukemic cells in vitro and in mice, and that this activity is dependent on its VEGFR-associated FV/FVIII domain. Finally, we show that treatment with VEGF inhibitor axitinib reduces AML cell growth and delays median leukemia latency in vivo. Our findings reveal that the NRP1/VEGF axis mediates proliferation in inv(16) AML blasts, and suggest that targeting NRP1 function could be promising in combination AML therapy.

2024-11-18 | GSE215613 | GEO

Genome wide N-MYC binding in human inv(16) AML cells

Project description:To identify the role of N-MYC in transcriptional regulation in human inv(16) AML, we conducted conducted CUT&Tag analysis for N-MYC and H3K27AC in ME-1 cells

2023-10-17 | GSE227930 | GEO

Mouse inv(16):TET2ko granulocyte macrophage progenitor (GMP) cells

Project description:inv(16)/Tet2-/- GMPs (Lin- Sca1- ckit+ CD41- FcgR+ CD150-) were FACS sorted as described in Supplementary Information (Reckzeh, K et al 2020) TET2 deficiency cooperates with CBFB-MYH11 to induce acute myeloid leukemia and represents an early leukemogenic event. Reckzeh, K et al.

2022-03-28 | GSE161390 | GEO

WT and inv(16)/KITD816Y granulocyte macrophage progenitor (GMP) cells [mouse]

Project description:WT GMPs (Lin- IL7R- Sca1- ckit+ FcgRhiCD34+) and inv(16)/KITD816Y GMPs (Lin- Sca1- ckit+ CD41- FcgR+ CD150-) were FACS sorted as described in material and methods from supplementary data (Estruch M et al 2020)

2020-11-09 | GSE150158 | GEO

Mouse inv(16):TET2ko granulocyte macrophage progenitor (GMP) cells

Project description:Mouse inv(16):TET2ko granulocyte macrophage progenitor (GMP) cells

| PRJNA678011 | ENA

Targeting miR-126 in inv(16) acute myeloid leukemia inhibits leukemia development and leukemia stem cell maintenance

Project description:Acute myeloid leukemia (AML) harboring inv(16)(p13q22) expresses high levels of miR-126. Here we show that the CBFB-MYH11 (CM) fusion gene upregulates miR-126 expression through aberrant miR-126 transcription and perturbed miR-126 biogenesis via the HDAC8/RAN-XPO5-RCC1 axis. Aberrant miR-126 upregulation promotes survival of leukemia-initiating progenitors and is critical for initiating and maintaining CM-driven AML. We show that miR-126 enhances MYC activity through the SPRED1/PLK2-ERK-MYC axis. Notably, genetic deletion of miR-126 significantly reduced AML rate and extended survival in CM knock-in mice. Therapeutic depletion of miR-126 with an anti-miR-126 (miRisten) inhibited AML cell survival, reduced leukemia burden and leukemia stem cell (LSC) activity in inv(16) AML murine and xenograft models. Combination of miRisten with chemotherapy further enhanced the anti-leukemia and anti-LSC activity. Overall, this study provides molecular insights for the mechanism and impact of miR-126 dysregulation in leukemogenesis and highlights the potential of miR-126 depletion as a new therapeutic approach for inv(16) AML.

2021-09-15 | GSE184015 | GEO

Addiction of t(8;21) and inv(16) AML to native RUNX1 [Gene Expression data]

Project description:Cancer cells maintain a sensitive balance between growth-promoting oncogenes and apoptosis inhibitors. We show that WT RUNX1 is required for survival of t(8;21)-Kasumi-1 and inv(16)-ME-1 AML cell lines. The malignant AML phenotype is sustained by a delicate AML1-ETO/RUNX1 balance that involves competition for common DNA binding sites regulating a subset of AML1-ETO/RUNX1 targets.

2013-08-18 | GSE45743 | GEO

Addiction of t(8;21) and inv(16) AML to native RUNX1 [ChIP-Seq data]

2013-08-18 | GSE45738 | GEO

Genome wide N-MYC binding in human inv(16) AML cells

Project description:Genome wide N-MYC binding in human inv(16) AML cells

| PRJNA947529 | ENA

WT and inv(16)/KITD816Y granulocyte macrophage progenitor (GMP) cells [mouse]

Project description:WT and inv(16)/KITD816Y granulocyte macrophage progenitor (GMP) cells [mouse]

| PRJNA631277 | ENA