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Affymetrix gene arrays of leukemic BM samples from 24 mice including 9 primary

ABSTRACT: To identify such targets of leukemia-related miRNAs such as miR-196b, we conducted Affymetrix gene arrays of leukemic BM samples from 24 mice including 9 primary (including 3 each of negative control, MLL-AF9, and miR-196b+MLL-AF9) and 15 secondary (including 3 negative control, 6 MLL-AF9, and 6 miR-196b+MLL-AF9) recipient mice

ORGANISM(S): Mus musculus

PROVIDER: GSE34185 | GEO | 2012/08/10

SECONDARY ACCESSION(S): PRJNA156373

REPOSITORIES: GEO

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Affymetrix gene arrays of leukemic BM samples from 24 mice including 9 primary

Project description:To identify such targets of leukemia-related miRNAs such as miR-196b, we conducted Affymetrix gene arrays of leukemic BM samples from 24 mice including 9 primary (including 3 each of negative control, MLL-AF9, and miR-196b+MLL-AF9) and 15 secondary (including 3 negative control, 6 MLL-AF9, and 6 miR-196b+MLL-AF9) recipient mice A total of 24 mouse bone marrow samples including 9 primary (including 3 each of negative control, MLL-AF9, and miR-196b+MLL-AF9) and 15 secondary (including 3 negative control, 6 MLL-AF9, and 6 miR-196b+MLL-AF9) obtained from the in vivo mouse bone marrow reconstitution assays were analyzed by use of Affymetrix GeneChip Mouse Gene 1.0 ST Array (Affymetirx, Santa Clara, CA)

2012-08-09 | E-GEOD-34185 | biostudies-arrayexpress

Screening microRNA-196 targets in 11q23-translocation acute myeloid leukemia reveal mechanisms maintaining leukemia stemness with therapeutic potential [RNA-seq]

Project description:microRNA are aberrantly expressed in acute myeloid leukemia (AML), and clinically may have diagnostic, prognostic, and therapeutic value. We identify one such microRNA, miR-196b, is essential for MLL-AF9 leukemia initiation and maintenance. To discover how miR-196b contributes to leukemogenesis, we utilized multiple unbiased approaches that identified and functionally screened miR-196b target activity in AML. Our studies resolved how conflicting networks of miRNA-regulated targets are integrated during leukemogenesis. This work uncovered two miR-196b direct targets, the cell cycle regulator Cdkn1b (p27Kip1) and Polycomb group member Phc2, that independently cooperate with MLL-AF9 to promote leukemogenesis by regulating stem cell transcriptional programs. Finally, we found that therapeutic disruption of miR-196b direct targeting of Cdkn1b suppresses leukemogenesis.

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MiR-150 Suppresses MLL-AF9 Associated Leukemia Through Simultaneously Targeting Multiple Oncogenes

Project description:This study report that miR-150, a key hematopoietic regulatory microRNA (miRNA) and one of the most downregulated miRNAs in MLL-associated leukemias, acts as a tumor suppressor to block the leukemogenic potency of leukemic stem cells. When expression of miR-150 was restored, a significantly suppressed leukemic stem cell potency of MLL-AF9 cells was observed both in vivo and in vitro. To investigate the tumor suppressive function of miR-150 in MLL-AF9 cells, we isolated three batches of MLL-AF9 cells infected with MDH empty vector or MDH-miR-150 expression retrovirus. Total RNA were extracted and applied for Agilent array analysis. Gene profiling analysis demonstrated that elevated miR-150 altered various aspects of gene expression patterns in MLL-AF9 cells, including stem cell signatures, cancer pathways, and cell survival. miR-150-MLL-AF9 and MDH-MLL-AF9 isolated cells were compared for gene expression patterns. Triplicates using three batches of FACS sorted cells were compared in pairs on the array. MDH-MLL-AF9 samples were labeld with Cy3 and miR-150-MLL-AF9 samples were labled with Cy5.

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MiR-150 Suppresses MLL-AF9 Associated Leukemia Through Simultaneously Targeting Multiple Oncogenes

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Affymetrix Human Exon 1.0 ST array assay of 15 human MLL-associated samples and 9 human normal bone marrow [HuEx-1_0-st]

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Project description:MLL-fusion proteins (MLL-FPs) are believed to maintain gene activation and induce mixed lineage leukemia (MLL) through aberrantly stimulating transcriptional elongation, but the underlying mechanisms are incompletely understood. Here we show that both MLL1 and AF9, one of the major fusion partners of MLL1, mainly occupy promoters and distal intergenic regions, exhibiting chromatin occupancy patterns resembling that of RNA polymerase II (Pol II) in HEL, a human cell line without MLL1 arrangement (MLLr). MLL1 and AF9 only co-regulate over a dozen genes despite of their co-occupancy on thousands of genes. They do not interact with each other, and their chromatin occupancy is also independent of each other. Moreover, AF9 deficiency in HEL cells decreases global TBP occupancy while decreases CDK9 occupancy on a small number of genes, suggesting an accessory role of AF9 in CDK9 recruitment and a possible major role in transcriptional initiation via initiation factor recruitment. Importantly, MLL1 and MLL-AF9 occupy promoters and distal intergenic regions, exhibiting identical chromatin occupancy patterns in MLL cells, and MLL-AF9 deficiency decreased occupancy of TBP and TFIIE on major target genes of MLL-AF9 in iMA9, a murine acute myeloid leukemia (AML) cell line inducibly expressing MLL-AF9, suggesting that it can also regulate initiation. These results suggest that there is no difference between MLL1 and MLL-AF9 with respect to location and size of occupancy sites, contrary to what people have believed, and that MLL-AF9 may also regulate transcriptional initiation in addition to widely-believed elongation.

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H3K9me3 ChIP-seq in MLL-rearranged leukemic stem cells and hematopoietic stem cells

Project description:Acute myeloid leukemia (AML) with rearrangement of the mixed-lineage leukemia (MLL) gene are the most aggressive hematopoietic malignancies. Previous studies demonstrated the distribution of several epigenetic modifications including H3K9me3, H3K79me2, H3K36me3, H3K4me3 and H3K27me3, in MLL-AF9 transformed murine cells. Here, we examined the H3K9me3 distribution in c-Kit+ cells (enriched with stem/progenitor cells) from both MLL-AF9 transformed murine cells in parallel with control wild-type cells, and found an overall lower distribution of H3K9me3 in leukemia stem cells than normal hematopoietic stem/progenitor cells.

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Affymetrix Human Exon 1.0 ST array assay of 15 human MLL-associated samples and 9 human normal bone marrow [HuEx-1_0-st]

Project description:To identify potential target genes of leukemia-related miRNAs such as miR-196b and miR-150 in human MLL-associated leukemia, we performed Affymetrix Human Exon 1.0 ST array assay of 15 human MLL-associated samples and 9 human normal bone marrow (including 3 each of CD34+, CD33+, and MNC) cell samples. A total of 15 MLL-associated (9 primary untreated leukemia and 6 leukemia cell line) samples and 9 human normal bone marrow samples (including 3 each of CD34+ hematopoietic stem/progenitor, CD33+ myeloid, and mononuclear cell (MNC) samples) were analyzed by use of Affymetrix Human Exon 1.0 ST arrays (Affymetirx, Santa Clara, CA).

2012-08-09 | E-GEOD-34184 | biostudies-arrayexpress

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Project description:Epigenetic changes in cancerous cells including alterations in histone methylation facilitate the installation of growth-promoting signaling networks by altering DNA accessibility to transcriptional machinery. The oncofusion protein MLL-AF9 promotes deviant histone methylation and induces acute myelogenous leukemia (AML) in animals. Despite observations supporting a role for WNT signaling in AML pathogenesis, we have a limited mechanistic account of how cancerous growth is sustained in this context. Using chemical antagonists of WNT signaling and genetic ablation of the WNT chaperone Wntless (Wls), we identified the homeobox domain gene Sine oculis 1 (Six1) to be an atypical WNT-controlled target gene in MLL-AF9-transformed leukemic stem cells (LSCs). Elimination of Wls or Six1 in MLL-AF9 LSCs, or their exposure to WNT pathway inhibitors results in extended survival in LSC-transplanted recipient mice suggesting that WNT/SIX1 signaling is critical to MLL-AF9 transformation. Profiling of chromatin accessibility changes using ATAC-seq of MLL-AF9 transformed cells reveals chromatin remodeling in Six1 DNA regions that support binding of the transcriptional effector TCF7L2. Our data suggests de novo installation of a WNT/SIX1 signaling axis is critical to the development of some forms of AML and reveals how epigenetic alterations can re-assemble master regulatory pathways controlling cell fate with cancer-promoting consequences.

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