Boswellic acid induced changes in gene expression and methylation in colorectal cancer cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Masanobu Takahashi
PROVIDER: E-GEOD-32276 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Genome wide DNA methylation profiling of colorectal cancer cell lines treated with acetyl-11-keto-β-boswellic acid (AKBA) or 5-aza-2’-deoxycytidine (DAC). The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across approximately 27,000 CpGs in the colorectal cancer cell line SW48. Samples included non-treated, AKBA-treated, and DAC-treated SW48 cells. Bisulphite converted DNA from the 3 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2
2012-12-01 | E-GEOD-32275 | biostudies-arrayexpress
Project description:Genome-wide analysis of boswellic acids-mediated gene regulation. The hypothesis tested in the present study was that boswellic acids up-regulate some subset of genes in part thorough demethylation of those promotor regions. Results provide important information on boswellic acids-mediated anti-cancer effects in human colon cancer. Total RNA obtained from the human colorectal cancer SW48 cells treated with DMSO alone or acetyl-11-keto-?-boswellic acid (AKBA).
2012-12-01 | E-GEOD-32274 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2012-12-18 | E-GEOD-40871 | biostudies-arrayexpress
Project description:The objective of the study was to characterize gene expression cascade involved in the suppression of B-cell activation and differentiation by 2,3,7,8-tetrachlorodibenzo-p-dixoxin (TCDD). The underlying hypothesis was that multiple nodes in the B-cell differentiation network are directly or indirectly regulated by TCDD through its receptor, the AHR. The mouse B-cell line (CH12.LX) was plated at 1X10^5 cells/ml at time 0 and activated with lipopolysaccharide (LPS, Salmonella typhosa). The cells were then treated with either dimethyl sulfoxide (DMSO, 0.01%) or 10 nM 2,3,7,8-tetrachlorodibenzo-p-dixoxin (TCDD). The cells were harvested at 0, 8, 12, 24, 36, and 48 hrs post-treatment. At the 0 hr time point, cells were untreated. A total of 4 experimental replicates per time point per treatment group were included with the cells for each replicate treated and harvested on separate days. Single color Affymetrix Mouse 430 2.0 arrays were used.
2010-10-21 | E-GEOD-21272 | biostudies-arrayexpress
Project description:Reversal of gene promoter DNA hypermethylation and associated abnormal gene silencing is an attractive approach to cancer therapy. The DNA methylation inhibitor, decitabine (5-aza-2'-deoxycitidine), is proving efficacious for hematological neoplasms especially at lower, less toxic, doses. Experimentally, high doses induce rapid DNA damage and cytotoxicity, but these may not explain the prolonged time to response seen in patients. Transient exposure of leukemic and solid tumor cells to clinically-relevant nanomolar doses, without causing immediate cytotoxicity or apoptosis, produces sustained reduced tumorigenicity, and for leukemia cells, diminished long-term self-renewal. These effects appear triggered by cellular reprogramming and include sustained decreases in promoter DNA methylation with associated gene re-expression, and anti-tumor changes in multiple key cellular regulatory pathways, most of which are high priority targets for pharmacologic anti-cancer strategies. Thus, low dose decitabine regimens appear to have broad applicability for cancer management. [Gene expression profiling] Leukemia cell lines Kasumi-1 and KG1A are treated with 10nM DAC during 72 hours and gene expression was assayed at day 3, 7 and 14 after the start of the treatment. Appropriate mock treated samples were used as control in each case. In addition, Kasumi-1 cells were also treated with a higher dose of DAC (500nM), 100nM ARA-C and 300 nM TSA, again controlled against mock treated Kasumi-1 cells, to separate dose and agent dependent effects. MCF7 was studied as an example of a solid tumor cell line. Therefore MCF7 cells were treated with 100nM DAC and results were assayed at day 1, day 3 and day 10. [Methylation profiling] The effects of the demethylating agent DAC were studied in the leukemia cell line Kasumi-1 over a 28 day time course. Intermediate time points were studied at days 3, 7, 14 and 21. These results were verfied in KG1A and KG1 leukemia cell lines, at one selected time point. The effects on one primary sample were also studied. Four normal leukemia samples (PL1, 2, 4 and 5) were used as general controls. The effect of DAC was compared to ARA-C, TSA. Both mock treated and day 3 DAC treated Kasumi-1 cells were repeated. These results were verified at one selected time point for the DAC treated MCF7 breast cancer cell line.
2012-03-21 | E-GEOD-20945 | biostudies-arrayexpress
Project description:We used bs-ATLAS-seq to comprehensively map the genomic location and assess the DNA methylation status of human full-length LINE-1 elements (L1). The approach is focused on the youngest family (L1HS), but it also catches a significant fraction of L1PA2 to L1PA8 elements. This was performed in HCT116 cells treated by the DNA methyltransferase inhibitor 5-aza-2’-deoxycytidine (5-aza) or in mock-treated cells (DMSO).
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Project description:Using label-free mass spectrometry, we measured phosphorylation changes in response to activation or inhibition of PI3K.
2016-07-22 | PXD003899 | Pride
Project description:We performed poly(A)+ stranded RNA-seq of a panel of the human colorectal adenocarcinoma cell line HCT-116 treated with 5-aza-2’-deoxycytidine. In parallel, we determined the genomic location and DNA methylation levels of human full-length LINE-1 elements (L1) from the same samples using bs-ATLAS-seq (E-MTAB-12240). To link DNA methylation and L1 expression, we used cell pellets from the same cell culture to perform both RNA-seq and bs-ATLAS-seq.
2023-09-21 | E-MTAB-12245 | biostudies-arrayexpress
Project description:The aryl hydrocarbon receptor (AHR) agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters differentiation of B cells and suppresses antibody production. The objectives of this study was to use a combination of whole genome, microarray-based chromatin immunoprecipitation (ChIP-on-chip) and time course gene expression microarray analysis on the mouse B-cell line CH12.LX following exposure to lipopolysaccharide (LPS) or LPS and TCDD to identify the primary and downstream transcriptional elements of B-cell differentiation that are altered by the AHR. CH12.LX cells (1X10^5 cells/ml, 25ml in P150s) were treated with either 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)(10nM) or vehicle (0.01% DMSO) for 1 hr and cells were fixed with 1% formaldehyde for 15 min and quenched with 0.125 M glycine. Chromatin was isolated by adding lysis buffer followed by disruption with a Dounce homogenizer. Lysates were sonicated and the DNA sheared to an average length of 300-500 bp. Genomic DNA was prepared by treating aliquots of chromatin with RNase, proteinase K and heat for de-crosslinking, followed by ethanol precipitation. Pellets were resuspended and the resulting DNA was quantified on a Nanodrop ND-1000 spectrophotometer. Extrapolation to the original chromatin volume allowed quantitation of the total chromatin yield. An aliquot of chromatin (30 ug) was precleared with protein - agarose beads. Factor-bound DNA sequences were isolated using antibodies against AhR (Biomol, Plymouth Meeting, PA, Catalog #: SA210-0100). After incubation at 4°C overnight, protein-agarose beads were used to isolate the immune complexes. Complexes were washed, eluted from the beads with SDS buffer, and subjected to RNase and proteinase K treatment. Crosslinks were reversed by incubation overnight at 65°C, and ChIP DNA was purified by phenol-chloroform extraction and ethanol precipitation. Following purification ChIP DNA was labeled, fragmented and hybridized to Affymetrix GeneChip Mouse Tiling 2.0 Array Sets, hybridized arrays were then washed and scanned using a GeneChip Fluidics Station 450 and a GeneChip 3000 scanner. The ChIP studies were performed in triplicate (n = 3) with the cells for each replicate treated and harvested on separate days.
2010-08-31 | E-GEOD-23708 | biostudies-arrayexpress
Project description:Acute myeloid leukemia (AML), and other myeloid malignancies, are frequently treated with hypomethylating agents like decitabine. Alterations in the epigenome, induced by decitabine, are likely to result in gene expression changes. The effects of decitabine have not been systemically studied using primary AML samples. We cultured 18 different primary AML samples for 7 days, the last 3 days of which included 100 nM decitabine (DAC) or 100 nm cytarabine (AraC). We hypothesized that decitabine treatment would result in detectable and consistent gene expression changes. For comparison, we also analyzed mRNA from cells treated with DMSO control (mock) and mRNA from uncultured cells taken at the time of diagnosis.
2012-12-18 | E-GEOD-40442 | biostudies-arrayexpress