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Epigenetic Control over IFN Type-I Response antagonizes self-renewal in acute myeloid leukemia (ChIP-seq)

ABSTRACT: Epigenetic Control over IFN Type-I Response antagonizes self-renewal in acute myeloid leukemia (ChIP-seq)

PROVIDER: PRJNA871241 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21138516.fastq.gz	Fastqsanger.gz
	SRR21138517.fastq.gz	Fastqsanger.gz
	SRR21138518.fastq.gz	Fastqsanger.gz
	SRR21138519.fastq.gz	Fastqsanger.gz
	SRR21138520.fastq.gz	Fastqsanger.gz

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Epigenetic control over IFN Type-I response antagonizes self-renewal in acute myeloid leukemia

Project description:Epigenetic control over IFN Type-I response antagonizes self-renewal in acute myeloid leukemia

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Project description:Epigenetic Control over IFN Type-I Response antagonizes self-renewal in acute myeloid leukemia (RNA-seq)

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Epigenetic Control over IFN Type-I Response antagonizes self-renewal in acute myeloid leukemia

Project description:Large biological heterogeneity hallmarks acute myeloid leukemia (AML) and substantially hampers development of novel comprehensive therapies. While all-trans retinoic acid (ATRA) revolutionized therapy of acute promyelocytic leukemia, its impact on other AML subtypes remained largely disappointing. Here we show for the first time that ATRA mediated phosphorylation of the histone demethylase PHF8 induces apoptosis of AML cells of different subtypes via regulation of viral mimicry and subsequent initiation of interferon (IFN) type-I response. Phospho-PHF8 conferred H3K9me2 demethylation at promoter sites of key initiators of cell-intrinsic immune response. Multiomics based analyses revealed activation of cytosolic RNA sensors as key step towards NF-κB driven IFN type-I mediated apoptosis. Epigenetic changes directed by PHF8 also induced a specific proteosome pathway controlling NF-κB activity after its initial activation. Hence, PHF8 orchestrates viral mimicry, triggering IFN type-I response-differentiation-apoptotic network in a broad spectrum of AML when activated by ATRA. Forced phosphorylation of PHF8 via combination treatment with ATRA and simultaneous pharmacological inhibition of PHF8 dephosphorylation significantly impaired growth of human AML. Our findings finally open the gate for successful application of ATRA-based combination therapies in AML.

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Asymmetric self-renewal associated (ASRA) genes

Project description:Cell lines geneticially engineered to undergo conditional asymmetric self-renewal were used to identify genes whose expression is asymmetric self-renewal associated (ASRA). Non-random sister chromatid segregation occurs concordantly with asymmetric self-renewal in these cell lines. Asymmetric self-renewal occurs when murine embryo fibroblasts that are otherwise p53-null are induced to express physiological levels of wildtype p53 protein (Asym). To distinguish p53-responsive genes that also require induction of asymmetric self renewal (i.e., ASRA genes) and/or non-random sister chromatid segregation for change, an additional control cell line, which continues to symmetrically self-renew (with random sister chromatid segregation) even when p53 is induced, was also compared (Symp53). This congenic cell line constitutively expresses the type II inosine monophosphate dehydrogenase (IMPDH II; the rate-limiting enzmye for guanine ribonucleotide biosynthesis) and, thereby, prevents p53-induced asymmetric self-renewal and non-random sister chromatid segregation. Three biological replicates of asymmetrically self-renewing cultures (Asym1-3) were compared with cultures that were symmetrically self-renewing - either because they did not express p53 (3 biological replicates, Sym1-3) or they expressed constitutive IMPDH II (i.e., not regulated by p53) as well as p53 (2 biological replicates, Symp53_1 and 2.)

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Project description:Previously, we identified the transcription factor Zfx as a key regulator of self-renewal in murine ESCs. Here we extend those findings to human ESCs. Zfx knockdown in hESCs hindered clonal growth and decreased colony size after serial replating. Zfx overexpression enhanced clone formation, increased colony size and decreased expression of differentiation-related genes in human ESCs. Zfx-overexpressing hESCs resisted spontaneous differentiation but could be directed to differentiate into endodermal and neural cell fates when provided with the appropriate cues. Thus, Zfx acts as a molecular rheostat regulating the balance between self-renewal and differentiation in hESCs, revealing the close evolutionary conservation of the self-renewal mechanisms in murine and human ESCs. Human embryonic stem cells with over expression of ZFX were compared to the original cell line (H9) and a clonally derived wild-type cell line (clone 3)

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Epigenetic control over IFN Type-I response antagonizes self-renewal in acute myeloid leukemia

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

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Project description:Mutations in the histone 3 variant H3.3 have been identified in one-third of pediatric glioblastomas (GBMs), but not in adult tumors. Here we show that H3.3 is a dynamic determinant of functional properties in adult GBM. H3.3 is repressed by mixed lineage leukemia 5 (MLL5) in self-renewing GBM cells. MLL5 is a global epigenetic repressor that orchestrates reorganization of chromatin structure by punctuating chromosomes with foci of compacted chromatin, favoring tumorigenic and self-renewing properties. Conversely, H3.3 antagonizes self-renewal and promotes differentiation. We exploited these epigenetic states to rationally identify two small molecules that effectively curb cancer stem cell properties in a preclinical model. Our work uncovers a role for MLL5 and H3.3 in maintaining self-renewal hierarchies in adult GBM.

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