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The Retinal Determination Gene Network can confer chemoresistant properties to AML

ABSTRACT: The Retinal Determination Gene Network can confer chemoresistant properties to AML

PROVIDER: PRJNA646306 | ENA |

REPOSITORIES: ENA

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The Retinal Determination Gene Network can confer chemoresistant properties to AML

Project description:The Retinal Determination Gene Network can confer chemoresistant properties to AML

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The Retinal Determination Gene Network can confer chemoresistant properties to AML

Project description:HoxA9, Six1 and Eya1 are targets of MOZ-TIF2 and MLL-AF9 fusion proteins in murine models. Hoxa9 overexpression can induce AML in murine HSPCs with a latency of ~6-9 months. Co-overexpression of RDGN members Six1 or Eya1 with Hoxa9 can enhance the differentiation block and colony forming potential of HoxA9 alone in vitro. RNA-seq was carried out on these lines to establish genetic pathways responsible for these chages in leukemogenicity. Benzarone is a potent EYA1 inhibitor. We wanted to assess if this drug was able to reverse the leukemogenic properties that EYA1 adds to HOXA9.

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The Retinal Determination Gene Network can confer chemoresistant properties to AML

Project description:Acute Myeloid Leukaemia (AML) is a highly heterogeneous disease characterised by an abnormal transcriptional landscape that results in a block in normal blood cell differentiation and aberrant self-renewal. Dysregulation of Homeobox A9 (HOXA9) expression is a hallmark of multiple AML subsets. Although HOXA9 is critical for maintaining leukaemic transformation, it has proven to be a challenging druggable target, and the underpinning molecular mechanisms through which it promotes leukaemogenesis remain elusive. Here, we report the existence of a dichotomous expression profile between sine oculis homeobox 1 SIX1 and the well known HOXA9 interactors MEIS1 in monocytic zinc finger (MOZ) and mixed-lineage leukaemia (MLL) rearranged AMLs. We employed ChIP-seq, together with RNA-seq, to identify regions bound and transcriptionally upregulated in a MOZ-TIF2 driven model of AML. Using RNA-seq, we demonstrated that SIX1 and EYA1 (the well known SIX1 partner) potentiates the transforming capacity of HOXA9 to confer a greater level of differentiation block via suppression of myelo-monocytic programmes. We next sought to define the impact of pharmacologically destabilising the EYA1/SIX1 complex using Benzarone. Through a single cell RNA-Seq timecourse following treatment of MOZ-TIF2 cells with Benzarone, we provide evidence that disruption of EYA1 and its interactions results in differentiation of these cells. To prove the specificity of Benzarone towards EYA1, we also conducted RNA-Seq on cells expressing EYA1 and HOXA9 or HOXA9 alone.

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