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

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

PROVIDER: PRJNA762718 | ENA |

REPOSITORIES: ENA

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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

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

Project description: Not available

| S-EPMC8536759 | biostudies-literature

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

miR-126 Governs Human Leukemia Stem Cell Quiescence and Therapeutic Resistance

Project description:In acute myeloid leukemia (AML), leukemia stem cells (LSC) play a central role in disease progression and recurrence due to their intrinsic capacity for self-renewal and chemotherapy resistance. Whereas epigenetic mechanisms balance normal blood stem cell self-renewal and fate decisions, mutation and dysregulation of epigenetic regulators are considered fundamental to leukemia initiation and progression. Alterations in miRNA function represent a non-canonical epigenetic mechanism influencing malignant hematopoiesis, however the function of miRNA in human LSC remains undetermined. Here we show that miRNA profiling of fractionated AML populations defines an LSC-specific signature that is highly prognostic for patient survival. Gain- and loss-of-function analyses demonstrated that miR-126 restrained cell cycle progression, prevented differentiation, and increased self-renewal of human LSC. By targeting the G0 to G1 gatekeeper CDK3, miR-126 preserved LSC quiescence and promoted chemotherapy resistance. Thus, in AML, miRNAs influence patient outcome through post-transcriptional regulation of stemness programs in LSC.

2016-03-31 | PXD001994 | Pride

Transcriptome Sequence Analysis of Pediatric Acute Megakaryoblastic Leukemia Identifies An Inv(16)(p13.3;q24.3)-Encoded CBFA2T3-GLIS2 Fusion Protein As a Recurrent Lesion in 39% of Non-Infant Cases

Project description:This SuperSeries is composed of the following subset Series: GSE35201: Transcriptome Sequence Analysis of Pediatric Acute Megakaryoblastic Leukemia Identifies An Inv(16)(p13.3;q24.3)-Encoded CBFA2T3-GLIS2 Fusion Protein As a Recurrent Lesion in 39% of Non-Infant Cases [2007] GSE35202: Transcriptome Sequence Analysis of Pediatric Acute Megakaryoblastic Leukemia Identifies An Inv(16)(p13.3;q24.3)-Encoded CBFA2T3-GLIS2 Fusion Protein As a Recurrent Lesion in 39% of Non-Infant Cases [2010] Refer to individual Series

2012-11-20 | E-GEOD-35203 | biostudies-arrayexpress

inv(16)/t(16;16) acute myeloid leukemia with non-type A CBFB-MYH11 fusions associate with distinct clinical and genetic features and lack KIT mutations

Project description:The inv(16)(p13q22)/t(16;16)(p13;q22) in acute myeloid leukemia results in multiple CBFB-MYH11 fusion transcripts, with type A being most frequent. The biologic and prognostic implications of different fusions are unclear. We analyzed CBFB-MYH11 fusion types in 208 inv(16)/t(16;16) patients with de novo disease, and compared clinical and cytogenetic features and KIT mutation status between type A (n=182; 87%) and non-type A (n=26; 13%) patients. We derived a fusion-type-associated gene- global expression profile. Gene Ontology analysis of the differentially expressed genes revealed - among others - an enrichment of up-regulated genes involved in activation of caspase activity, cell differentiation and cell cycle control in non-type A patients.

2013-01-23 | E-MTAB-1356 | biostudies-arrayexpress

Vibrio cholerae strain:V-126-16 | isolate:V-126-16

Project description:Vibrio cholerae strain:V-126-16 | isolate:V-126-16 Genome sequencing and assembly

| PRJNA378296 | ENA

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

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

Changed gene profile in inv cystic kidney

Project description:Nephronophthisis (NPHP) is a group of progressive renal disorders characterized by a variable number of cysts associated with cortical tubular atrophy. Recently, mutations in INV have been identified to be responsible for NPHP2. The inv/inv,inv-deltaC::GFP mouse that was created by introduction of inv gene lacking the C-terminus (inv-deltaC) into inv/inv mice develops multiple renal cysts without situs abnormality. Renal cyst progression was dependent on expression level of inv-deltaC transgene, suggesting that inv protein functions in a dose-dependent manner. Cell proliferation and apoptosis were increased in the inv-deltaC cystic kidneys. We searched up- and down-regulated genes during cyst development and progression using cDNA microarray. See appended table for comparison analysis of inv/inv,inv-deltaC::GFP vs +/+,inv-deltaC::GFP (GSM100334 vs GSM100335). Keywords: apoptosis, cell proliferation, gene expression, inv, inversin, polycystic kidney disease

2006-05-01 | GSE4462 | GEO

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