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Alcohol-abuse drug disulfiram targets pediatric glioma via MLL degradation

ABSTRACT: RNA-seq analysis was performed to compare gene expression of glioma cells with MLL1 and MLL2 knockdown, and control glioma cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE139016 | GEO | 2019/12/20

REPOSITORIES: GEO

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Alcohol-abuse drug disulfiram targets pediatric glioma via MLL degradation.

Project description: Not available

| S-EPMC8358054 | biostudies-literature

Alcohol-abuse drug disulfiram targets pediatric glioma via MLL degradation

Project description:Alcohol-abuse drug disulfiram targets pediatric glioma via MLL degradation

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Effect of disulfiram treatment on pediatric high grade glioma

Project description:RNA-seq analysis was performed to compare gene expression between glioma cells treated with disulfiram and untreated glioma cells.

2019-10-16 | GSE138863 | GEO

MLL2, but not MLL1, plays a major role to sustain leukemia survival [RNA-seq]

Project description:We investigated the effect of Mll1, Mll2 and Mll1;Mll2 deletion on gene expression in MLL-AF9-transformed cells.

2017-01-20 | GSE93622 | GEO

Multi-omics analysis of MEN1 missense mutations identifies disruption of menin-MLL and menin-JunD interactions as critical requirements for molecular pathogenicity

Project description:Loss-of-function mutations of the multiple endocrine neoplasia type 1 (MEN1) gene are causal to the MEN1 tumor syndrome, but they are also commonly found in sporadic pancreatic neuroendocrine tumors and other types of cancers. The MEN1 gene product, menin, is involved in transcriptional and chromatin regulation, most prominently as an integral component of KMT2A/MLL1 and KMT2B/MLL2 containing COMPASS-like histone H3K4 methyltransferase complexes. In a mutually exclusive fashion, menin also interacts with the JunD subunit of the AP-1 and ATF/CREB transcription factors. After in silico screening of 253 disease-related MEN1 missense mutations, we selected a set of nine menin mutations in surface-exposed residues. The protein interactomes of these mutants were assessed by quantitative mass spectrometry, which indicated that seven of the nine mutants disrupt interactions with both MLL1/2 and JunD complexes in the nucleus. We identified three missense mutations, R52G, E255K and E359K, which display predominant reduction in interaction with MLL1 compared to JunD. This observation was supported by a pronounced loss of binding of the R52G, E255K and E359K mutant proteins at unique MLL1 genomic binding sites with less effect on unique JunD sites. These findings support the general importance of the menin-MLL1 and menin-JunD interactions in MEN1 gene-associated pathogenic conditions.

2022-10-14 | PXD031928 | Pride

Effect of disulfiram treatment on pediatric high grade glioma

Project description:Effect of disulfiram treatment on pediatric high grade glioma

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Alcohol-abuse drug disulfiram targets cancer via p97 segregase adaptor NPL4.

Project description: Not available

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Regulation of transcription by MLL2 complex and MLL complexes-associated protein AKAP95

Project description:Although histone H3 lysine 4 (H3K4) methylation is widely associated with gene activation, direct evidence for its causal role in transcription, through specific MLL family members, is scarce. Here we have purified a human MLL2 (Kmt2b) complex that is highly active in H3K4 methylation and chromatin transcription in a cell-free system. This effect requires SAM and intact H3K4, establishing a direct and causal role for MLL2-mediated H3K4 methylation in transcription. We then show that human AKAP95, a chromatin-associated protein, is physically and functionally associated with the Dpy-30-MLL complexes and directly enhances their methyltransferase activity. Ectopic AKAP95 stimulates expression of a chromosomal reporter in synergy with MLL1 or MLL2, whereas AKAP95 depletion impairs retinoic acid-mediated gene induction in embryonic stem cells. These results demonstrate an important role for AKAP95 in regulating histone methylation and gene expression, particularly during cell fate transitions. Total RNAs from control or knockdown cells before and after RA-mediated differentiation were subjected to Illumina microarray analyses. The complete dataset containing non_normalized, median-normalized and expression ratio (relative to Scramble shRNA, undifferentiated data) is linked below as a supplementary file [complete_data.txt].

2013-07-01 | E-GEOD-48128 | biostudies-arrayexpress

MLL2, but not MLL1, plays a major role to sustain leukemia survival [array]

Project description:The MLL1 histone methyltransferase gene undergoes many distinct chromosomal rearrangements to yield poor-prognosis leukemia. The remaining wild-type allele is most commonly, but not always, retained. To what extent the wild-type allele contributes to leukemogenesis is unclear. Here we show using rigorous, independent animal models that endogenous MLL1 is dispensable for MLL-rearranged leukemia. Potential redundancy was addressed by co-deleting the closest paralog, Mll2. Surprisingly, Mll2 deletion alone had a significant impact on survival of MLL-AF9-transformed cells and additional Mll1 loss further reduced viability and proliferation. We show that MLL1/MLL2 collaboration is not through redundancy but regulation of distinct pathways. These findings highlight the relevance of MLL2 as a drug target in MLL-rearranged leukemia and suggest its broader significance in AML. We used microarray to investigate the effect of Mll1 deletion on gene expression in LSC-enriched MLL-AF9 leukemia cells.

2017-01-20 | GSE93621 | GEO

Regulation of transcription by MLL2 complex and MLL complexes-associated protein AKAP95

2013-07-01 | GSE48128 | GEO

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