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DNA methylome analysis of DNA methyltransferase inhibitor reagent-treated lung cancer cells

ABSTRACT: DNA methylome analysis of DNA methyltransferase inhibitor reagent-treated lung cancer cells

PROVIDER: PRJNA607680 | ENA |

REPOSITORIES: ENA

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DNA methylome analysis of DNA methyltransferase inhibitor reagent-treated lung cancer cells

Project description:Purpose: Epigenetic drug DNA methyltransferase inhibitors (DNMTis) are immunomodulating agents that may sensitize cancer cells to immune cell attack. However, it is still unclear how DNMTi affects cancer cells to the killing by immune cells. We therefore try to uncover the alternations of genomic DNA methylation after DNMTi treatment of cancer cells. Methods: Six human lung cancer cell lines (A549, H1299, CL1-0, CL1-5, H1792, PC9) before (Mock) and after (DAC) treatement with 100 nM decitabine (DAC) for 72 hours followed by growing in drug-free medium for three days were subjected to Illumina MethylationEPIC microarray analysis. Results: DNA methylome analysis reveals DNMTi-induced DNA demethylation at transcription start site (TSS)-flanking regions of several actin, intermediate filament and microtubule molecules in human lung cancer cell lines. Conclusion: Decitabine primes lung cancer cells to γδ T cell-mediated killing through regulating cytoskeleton associated genes potentially involved in immune synapse formation.

2021-02-16 | GSE145588 | GEO

Transcription profiling of primary cultured ovarian cells and ovarian cancer cell lines in the presence and absence of a DNA methyltransferase inhibitor

Project description:This SuperSeries is composed of the following subset Series: GSE25427: Gene expression profiles of primary cultured ovarian cells in the presence and absence of a DNA methyltransferase inhibitor GSE25428: Gene expression profiles of ovarian cancer cell lines in the presence and absence of a DNA methyltransferase inhibitor Refer to individual Series

2010-11-17 | E-GEOD-25429 | biostudies-arrayexpress

DNA Methyltransferase Inhibitor Zebularine Induces Human Cholangiocarcinoma Cell Death through Alteration of DNA Methylation Status

Project description:Cholangiocarcinoma (CCA) is a cancer arising from the neoplastic transformation of cholangiocytes. During tumorigenesis, tumor suppressor and cancer-related genes are commonly silenced by aberrant DNA methylation in their promoter regions. Zebularine (1-(β-D-ribofuranosyl)-1,2-dihydropyrimidin-2-one) acts as an inhibitor of DNA methylation and exhibits chemical stability and minimal cytotoxicity both in vitro and in vivo. In this study, we explore the effect and possible mechanism of action of zebularine on CCA cells. We demonstrate that zebularine exerts an antitumor effect on CCA cells. Zebularine treatment decreased the concentrations of DNA methyltransferase (DNMT) proteins, and DNMT1 knockdown led to apoptotic cell death in the CCA cell lines TFK-1 and HuCCT1. DNA methylation analysis demonstrated that zebularine induced DNA demethylation, and the GO Biological Process terms “hemophilic cell adhesion”, “regulation of transcription, DNAdependent” and “Wnt signaling pathway” were found to be significantly enriched in association with demethylated genes. Furthermore, we observed that zebularine treatment decreased β-catenin protein levels in TFK-1 and HuCCT1 cells. These results suggest that zebularine alters DNA methylation status, and that some aspect of DNA demethylation by zebularine induces suppression of the Wnt signaling pathway, which leads to apoptotic cell death in CCA. We previously reported a novel mechanism of zebularine-induced cell growth arrest and apoptosis in hepatocellular carcinoma via a DNA methylation-independent pathway. Together, our present and previous studies indicate that zebularine could function as both a DNMT inhibitor and a non-DNMT inhibitor reagent, and that, while the optimal usage of zebularine may depend on cancer type, zebularine may be useful for chemotherapy against cancer.

2015-03-24 | GSE60446 | GEO

DNA methylome of pineapple

Project description:DNA methylome of pineapple

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The Helicobacter pylori Methylome is Acid-Responsive due to Regulation by the Two-Component System ArsRS and the Type I DNA Methyltransferase HsdM1 (HP0463)

Project description:Helicobacter pylori colonizes the gastric epithelium and is the leading cause of gastric adenocarcinoma. There is increasing evidence that DNA methylation regulates gene expression in addition to its role in genome protection. In this study, we characterize the impact of acidity, the Two-Component System (TCS) ArsRS, Autoinducer-2, and the Type I m6A DNA methyltransferase HsdM1 (HP0463) on the Helicobacter pylori methylome. Transcription of hsdM1 increases at least 4-fold in the absence of the sensory histidine kinase ArsS, the major acid sensing protein of H. pylori. HsdM1 exists in the phase-variable operon hsdR1-hsdM1. Phase-locking hsdR1 (HP0464), the restriction endonuclease gene, has significant impacts on the transcription of hsdM1. To determine the impacts of methyltransferase transcription patterns on the methylome, we conducted methylome sequencing on samples that had undergone prolonged acid-exposure experiment. We found differentially methylated motifs between pH 7 and pH 5 growth conditions, and that deletions of arsS and hsdM1 interfere with the epigenetic acid response. Deletion of arsS leads to altered hsdM1 expression and alters the activity of multiple methyltransferases in both conditions indicating that the ArsRS TCS, in addition to its role in acid acclimation via direct effects on regulon member transcription, may also indirectly impact gene expression via regulation of the methylome. We characterized the target motif of HsdM1 (HP0463) to be (H)HTCAVN6TGY. HsdM1 may hierarchically regulate the Type II m5C DNA methyltransferase HP1121. This complex regulation of DNA methyltransferases, and thus differential methylation patterns, may have implications for the decades-long persistent infection by H. pylori.

2024-01-01 | GSE241991 | GEO

Transcription profiling of 4 prostate cancer cell lines treated with the DNA methyltransferase inhibitor 5-aza-dC

Project description:This microarray dataset accompanies the publication by Kim et al, "The retinoic acid synthesis gene ALDH1a2 is a candidate tumor suppressor in prostate cancer". The dataset comprises four prostate cancer cell lines treated with the DNA methyltransferase inhibitor 5-aza-dC. For each cell line, gene expression in treated (channel 2; Cy5) and untreated (channel 1; Cy3) cells is directly compared by hybridization to the same DNA microarray. Further details on the treatment conditions are provided in the manuscript.

2005-10-18 | E-SMDB-3416 | biostudies-arrayexpress

DNA methyltransferase inhibitor 5-aza-dC-treated prostate cancer cell lines

2006-01-25 | GSE4089 | GEO

DNA methylation profile for male SD rats treated with high fat diet (HFD) and DNA methyltransferase (DNMT) inhibitor 5-aza-2′-deoxycytidine (5-AzaD) by RRBS

Project description:To investigate the effects of HFD on affecting the DNA methylation, as well as the methylation inhibitor 5-AzaD reversing such effects in the frontal cortex of male SD rats by sequencing the methylome (RRBS).

2017-12-31 | GSE64948 | GEO

DNA methylome of tea tree

Project description:DNA methylome of tea tree

| PRJNA491190 | ENA

Integrative Epigenetic Analysis Reveals Therapeutic Targets to the DNA Methyltransferase Inhibitor SGI-110 in Hepatocellular Carcinoma Cells [gene expression]

Project description:There is an urgent need for developing more effective therapies for aggressive hepatocellular carcinoma (HCC). Guadecitabine (SGI-110) is a second-generation DNA methyltransferase inhibitor (DNMTi) currently in clinical trials for HCC and shows greater stability and performance over first generation DNMTis. The aim of this study is to identify potential therapeutic targets of SGI-110 for clinical trials.

2018-06-26 | GSE105065 | GEO

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