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Combinatorial treatment of DNMT inhibitor and LSD1 inhibitor results in cell growth inhibition and reexpression of epigenetically silenced genes (methylation)

ABSTRACT: A combinatorial treatment consisting of a DNMTi and a LSD1i shows synergistic effects in reactivating aberrantly silenced genes by enriching H3K4me2 and H3K4me. Bisulphite converted DNA from the 8 samples were hybridised to the Illumina Infinium HM450 Human Methylation Beadchip

ORGANISM(S): Homo sapiens

SUBMITTER: Xiaojing Yang

PROVIDER: E-GEOD-41525 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Combinatorial treatment of DNMT inhibitor and LSD1 inhibitor results in cell growth inhibition and reexpression of epigenetically silenced genes (gene expression)

Project description:A combinatorial treatment consisting of a DNMTi and a LSD1i shows synergistic effects in reactivating aberrantly silenced genes by enriching H3K4me2 and H3K4me. 24 Samples consisting of 3 cell lines hybridised to the Illumina HumanHT-12 V4.0 Beadchip.

2013-08-01 | E-GEOD-41676 | biostudies-arrayexpress

Combinatorial treatment of DNMT inhibitor and LSD1 inhibitor results in cell growth inhibition and reexpression of epigenetically silenced genes (methylation)

Project description:A combinatorial treatment consisting of a DNMTi and a LSD1i shows synergistic effects in reactivating aberrantly silenced genes by enriching H3K4me2 and H3K4me.

2013-08-01 | GSE41525 | GEO

Combinatorial treatment of DNMT inhibitor and LSD1 inhibitor results in cell growth inhibition and reexpression of epigenetically silenced genes (gene expression)

Project description:A combinatorial treatment consisting of a DNMTi and a LSD1i shows synergistic effects in reactivating aberrantly silenced genes by enriching H3K4me2 and H3K4me.

2013-08-01 | GSE41676 | GEO

Combinatorial treatment of DNMT inhibitor and LSD1 inhibitor results in cell growth inhibition and reexpression of epigenetically silenced genes

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-08-01 | E-GEOD-41754 | biostudies-arrayexpress

Gene Body Methylation Directly Increases Gene Expression and is a Therapeutic Target for Genes Upregulated in Cancer (methylation)

Project description:Demethylation treatment reduce gene body methylation as well as gene expression Bisulphite converted DNA from the 22 samples were hybridised to the Illumina Infinium HM450 Human Methylation Beadchip

2014-08-01 | E-GEOD-51810 | biostudies-arrayexpress

Combinatorial treatment of DNMT inhibitor and LSD1 inhibitor results in cell growth inhibition and reexpression of epigenetically silenced genes

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

2013-08-01 | GSE41754 | GEO

scRNAseq analysis of lytically and latently infected KSHV-infected iSLK.219 cells with and without caspase inhibitor treatment

Project description:The goal of this analysis was to examine the cell-to-cell variation in Kaposi's sarcoma-associated herpesvirus (KSHV) reactivation and type I interferon response after caspase inhibitor treatment. We profiled the levels of host and viral mRNAs at a single-cell level using the iSLK.219 tissue culture model system (Myoung and Ganem, 2011). We examined gene expression in lytically reactivating cells, lytically reactivating cells treated with caspase inhibitors, and lytically reactivating cells treated with casapse inhibitors and neutralizing antibodies against interferons. (we previously described that caspase inhibitors elicit an interferion response in KSHV-infected cells, Tabtieng et al., 2018). We also examined gene expression in a mixture of latently infected cells and uninfected cells as a control.

2022-09-29 | GSE190558 | GEO

Emerging Advances in Combinatorial Treatments of Epigenetically Altered Pediatric High-Grade H3K27M Gliomas.

Project description:Somatic mutations in histone encoding genes result in gross alterations in the epigenetic landscape. Diffuse intrinsic pontine glioma (DIPG) is a pediatric high-grade glioma (pHGG) and one of the most challenging cancers to treat, with only 1% surviving for 5 years. Due to the location in the brainstem, DIPGs are difficult to resect and rapidly turn into a fatal disease. Over 80% of DIPGs confer mutations in genes coding for histone 3 variants (H3.3 or H3.1/H3.2), with lysine to methionine substitution at position 27 (H3K27M). This results in a global decrease in H3K27 trimethylation, increased H3K27 acetylation, and widespread oncogenic changes in gene expression. Epigenetic modifying drugs emerge as promising candidates to treat DIPG, with histone deacetylase (HDAC) inhibitors taking the lead in preclinical and clinical studies. However, some data show the evolving resistance of DIPGs to the most studied HDAC inhibitor panobinostat and highlight the need to further investigate its mechanism of action. A new forceful line of research explores the simultaneous use of multiple inhibitors that could target epigenetically induced changes in DIPG chromatin and enhance the anticancer response of single agents. In this review, we summarize the therapeutic approaches against H3K27M-expressing pHGGs focused on targeting epigenetic dysregulation and highlight promising combinatorial drug treatments. We assessed the effectiveness of the epigenetic drugs that are already in clinical trials in pHGGs. The constantly expanding understanding of the epigenetic vulnerabilities of H3K27M-expressing pHGGs provides new tumor-specific targets, opens new possibilities of therapy, and gives hope to find a cure for this deadly disease.

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AID downregulation is a novel function of the DNMT inhibitor 5-aza-deoxycytidine.

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PBRM1 Deficiency Sensitizes Renal Cancer Cells to DNMT Inhibitor 5-Fluoro-2'-Deoxycytidine.

Project description:PBRM1 is a tumor suppressor frequently mutated in clear cell renal cell carcinoma. However, no effective targeted therapies exist for ccRCC with PBRM1 loss. To identify novel therapeutic approaches to targeting PBRM1-deficient renal cancers, we employed a synthetic lethality compound screening in isogenic PBRM1+/+ and PBRM1-/- 786-O renal tumor cells and found that a DNMT inhibitor 5-Fluoro-2'-deoxycytidine (Fdcyd) selectively inhibit PBRM1-deficient tumor growth. RCC cells lacking PBRM1 show enhanced DNA damage response, which leads to sensitivity to DNA toxic drugs. Fdcyd treatment not only induces DNA damage, but also re-activated a pro-apoptotic factor XAF1 and further promotes the genotoxic stress-induced PBRM1-deficient cell death. This study shows a novel synthetic lethality interaction between PBRM1 loss and Fdcyd treatment and indicates that DNMT inhibitor represents a novel strategy for treating ccRCC with PBRM1 loss-of-function mutations.

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