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The Mechanistic Differences/Similarities of Azacitidine and Decitabine in Models of Mature T-cell Lymphoma

ABSTRACT: We perform expression analysis on a panel of three T-cell lymphoma lines exposed to 5-azacytidine and decitabine as single agent.

ORGANISM(S): Homo sapiens

PROVIDER: GSE159925 | GEO | 2020/10/24

REPOSITORIES: GEO

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The Mechanistic Differences/Similarities of Azacitidine and Decitabine in Models of Mature T-cell Lymphoma

Project description:The Mechanistic Differences/Similarities of Azacitidine and Decitabine in Models of Mature T-cell Lymphoma

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Methylation profiling by array of human cell line HCT116 after treatment with demethylating drugs azacytidine or decitabine.

Project description:array-based analysis of genome-wide DNA methylation changes induced by the demethylating drugs azacytidine and decitabine on HCT116 cells for 24 hours

2010-07-01 | E-MTAB-210 | biostudies-arrayexpress

Methylation profiling by array of human HCT116 and HL60 cells treated with the demthylating drugs azacytidine and decitabine

Project description:Array-based analysis of genome-wide DNA methylation changes induced by the demethylating drugs azacytidine and decitabine on HCT116 and HL60 cells for 24 hours

2010-12-01 | E-MTAB-417 | biostudies-arrayexpress

The type of DNA damage response after Decitabine treatment depends on the level of DNMT activity

Project description:Decitabine and Azacytidine are considered as epigenetic drugs that induce DNA-methyltransferase (DNMT)-DNA crosslinks, resulting in DNA-hypomethylation and -damage. Although they are already applied against myeloid cancers, important aspects of their mode of action remain unknown, highly limiting their clinical potential. Using a combinatorial approach, we reveal that the efficacy profile of both compounds primarily depends on the level of induced DNA-damage. Under low DNMT-activity, only Decitabine has a substantial impact. Conversely, when DNMT-activity is high, toxicity and cellular response to both compounds are dramatically increased, but do not primarily depend on DNA-hypomethylation or RNA-associated processes. By investigating proteome dynamics on chromatin, we show that Decitabine induces a strictly DNMT-dependent multifaceted DNA-damage response based on chromatin-recruitment, but not expression level changes of repair-associated proteins. The choice of DNA-repair pathway herby depends on the severity of Decitabine-induced DNA-lesions. While under moderate DNMT-activity, mismatch (MMR), base-excision (BER) and Fanconi anemia-dependent DNA-repair combined with homologous recombination are activated in response to Decitabine, high DNMT-activity and therefore immense replication stress, induce activation of MMR and BER followed by non-homologous end-joining.

2024-06-19 | PXD045353 | Pride

Transcriptomic profiling of KMT2A-rearranged infant acute lymphoblastic leukemia (ALL) cells after treatment witith azacitidine and decitabine.

Project description:Transcriptomic profiling was performed on six cell lines derived from infants with KMT2A-rearranged ALL following treatment with two hypomethylating drugs (azacitidine and decitabine) administered at low doses for 72 hours in vitro. We identified changes in gene expression following treatment with hypomethylating agents, with decitabine exerting a greater effect than azacitidine.

2022-12-31 | GSE212591 | GEO

Gene expression profile of azacitidine- and decitabine- resistant HTLV-1-infected cell lines

Project description:We generated azacitidine (AZA)- and decitabine (DAC)-resistant (AZA-R and DAC-R, respectively) cells from drug-sensitive ATL cell lines TL-Om1 and MT-2 via long-term drug exposure. To identify molecular mechanisms responsible for acquired resistance, we performed transcriptome analysis using Clariom S microarray.

2021-11-30 | GSE166980 | GEO

Genome-wide methylation profiling of KMT2A-rearranged infant Acute Lymphoblastic Leukemia (ALL) cells after treatment with azacitidine, decitabine and zebularine

Project description:Genome-wide methylation profiling was performed on six cell lines derived from infants with KMT2A-rearranged ALL following treatment with three hypomethylating drugs (azacitidine, decitabine and zebularine) administered at low doses for 72 hours in vitro. We identified drug-specific and common differentially methylated regions and validated differentially expressed genes located within such regions, indicating commonalities in pathways targeted by azacitidine and decitabine in KMT2A-rearranged infant ALL. Of the three drugs, the most significant degree of hypomethylation was induced by decitabine followed by azacitidine, whereas zebularine did not exert a significant hypomethylating effect.

2022-12-31 | GSE198679 | GEO

Increasing of antitumor effect of decitabine against classical Hodgkin lymphoma (cHL) by targeting decitabine-activated pro-survival pathways

Project description:We found that 5-Aza-dC/decitabine induces various prosurvival pathways (JAK-STAT-, NFkB-, MEK/ERK- and PI3K/AKTpathway) in cHL cell lines. Inhibition of these pathways with specific small molecular weight inhibitors potentiates the antitumor effect of 5-Aza-dC.

2017-08-01 | GSE86068 | GEO

Expression data comparing azacitidine and decitabine in non-small cell lung cancer lines

Project description:Azacitidine (AZA) and decitabine (DAC) are cytidine azanucleoside analogs with clinical activity in myelodysplastic syndromes (MDS) and potential activity in solid tumors. To better understand the mechanism of action of these drugs, we examined the effects of AZA and DAC in a panel of non-small cell lung cancer (NSCLC) cell lines. Of 5 NSCLC lines tested in a cell viability assay, all were sensitive to AZA (EC50 of 1.8M-bM-^@M-^S10.5 M-BM-5M), while only H1299 cells were equally sensitive to DAC (EC50 of 5.1 M-BM-5M). In the relatively DAC-insensitive cell line A549, both AZA and DAC caused DNA methyltransferase I depletion and DNA hypomethylation; however, only AZA significantly induced markers of DNA damage and apoptosis, suggesting that mechanisms in addition to, or other than, DNA hypomethylation are important for AZA-induced cell death. Cell cycle analysis indicated that AZA induced an accumulation of cells in sub-G1 phase, whereas DAC mainly caused an increase of cells in G2/M. Gene expression analysis of AZA- and DAC-treated cells revealed strikingly different profiles, with many genes distinctly regulated by each drug. In summary, while both AZA and DAC caused DNA hypomethylation, distinct effects were demonstrated on regulation of gene expression, cell cycle, DNA damage, and apoptosis. A549 and H1299 cells were treated with a dose range (0.3M-bM-^@M-^S3.0 M-NM-<M) of AZA or DAC for 48 hours, and effects on gene expression were assessed by microarray analysis.

2011-05-05 | E-GEOD-29077 | biostudies-arrayexpress

SUM159 BrCa Decitabine Gene Expression

Project description:Dysregulation of DNA methylation is an established feature of breast cancers. DNA demethylating therapies like decitabine are proposed for the treatment of triple-negative breast cancers (TNBCs) and indicators of response need to be identified. For this purpose, we characterized the effects of decitabine in a panel of 10 breast cancer cell lines and observed a range of sensitivity to decitabine that was not subtype-specific. Knockdown of potential key effectors demonstrated the requirement of deoxycytidine kinase (DCK) for decitabine response in breast cancer cells. In treatment-naive breast tumors, DCK was higher in TNBCs, and DCK levels were sustained or increased post chemotherapy treatment. This suggests that limited DCK levels will not be a barrier to response in TNBC patients treated with decitabine as a second line treatment or in a clinical trial. Methylome analysis revealed that genome-wide, region-specific, tumor suppressor gene-specific methylation, and decitabine-induced demethylation did not predict response to decitabine. Gene set enrichment analysis (GSEA) of transcriptome data demonstrated that decitabine induced genes within apoptosis, cell cycle, stress, and immune pathways in decitabine treated cells. Induced genes included those characterized by the viral mimicry response; however knockdown of key effectors of the pathway did not affect decitabine sensitivity suggesting that breast cancer growth suppression by decitabine is independent of viral mimicry. Finally, taxol-resistant breast cancer cells expressing high levels of multidrug resistance transporter ABCB1 remained sensitive to decitabine, suggesting that the drug could be used as second-line treatment for chemoresistant patients. We used microarrays to determine genome-wide expression changes induced by DNA de-methylating agent decitabine in breast cancer cell lines

2020-06-01 | GSE133987 | GEO

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