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Treatment of prostate cancer cells with S-adenosylmethionine leads to genomewide alterations of transcription profiles.

ABSTRACT: The analysis investigates the impact of methyl donor S-adenosylmethionin on transcription and methylation profiles of prostate carcinoma cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE71303 | GEO | 2015/07/25

SECONDARY ACCESSION(S): PRJNA290863

REPOSITORIES: GEO

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Treatment of prostate cancer cells with S-adenosylmethionine leads to genomewide alterations of transcription profiles

Project description:The analysis investigates the impact of methyl donor S-adenosylmethionin on transcription and methylation profiles of prostate carcinoma cells.

2015-07-18 | GSE71070 | GEO

Treatment of prostate cancer cells with S-adenosylmethionine leads to genomewide alterations of transcription profiles.

Project description:The analysis investigates the impact of methyl donor S-adenosylmethionin on transcription and methylation profiles of prostate carcinoma cells. PC-3 cells (Prostatecarcinoma cells) were treated with 160 micromolar S-adenosylmethionine or vehicle

2015-07-25 | E-GEOD-71303 | biostudies-arrayexpress

S-adenosylmethionine (SAM) treatment attenuates breast cancer growth, invasion, metastasis

Project description:This study examines the therapeutic plausibility of using universal methyl group donor S-adenosylmethionine (SAM) to block breast cancer development, growth, and metastasis. cancer. Anti-tumor and anti-metastatic activity of SAM was evaluated through a series of studies in vitro using two different human breast cancer cell lines and in vivo using a MDA-MB-231 xenograft model of breast cancer. The data shown in this array is obtained from control and SAM-treated MDA-MB-231 cell lines.

2017-04-28 | GSE98275 | GEO

S-adenosylmethionine treatment affects histone methylation in prostate cancer cells

Project description:S-adenosylmethionine represents a potent inhibitor of cancer cell proliferation, migration and invasion in vitro. The reason remains unclear. Here, we examined if treatment with exogenous SAM is capable of causing alterations in the methylation of the histone markers H3K4me3 and H3K27me3, which are both known to be important in the initiation and progression of prostate cancer.

2023-10-26 | GSE235629 | GEO

S-adenosylmethionine treatment affects histone methylation in prostate cancer cells

Project description:S-adenosylmethionine treatment affects histone methylation in prostate cancer cells

| PRJNA986576 | ENA

S-adenosylmethionine (SAM) changes DNA methylation patterns in prostate cancer cells

Project description:Genome-wide DNA methylation profiling of human PC3 invasive prostate cancer cell line treated with vehicle control (SAH, S-adenosylhomocysteine) and with SAM (S-adenosylmethionine) as well as of untreated human LNCaP non-invasive prostate cancer cell line. The Illumina Infinium 450k Human DNA Methylation BeadChip v1.2 was used to obtain DNA methylation profiles across approximately 450,000 CpGs in human cell lines exposed to described treatments. Samples included biological triplicate of PC3 control (SAH treated), biological triplicate of PC3 treated with SAM, and biological duplicate of LNCaP untreated. Bisulfite-converted DNA from the 8 samples were hybridised to the Illumina Infinium 450k Human Methylation BeadChip v1.2.

2015-03-01 | E-GEOD-62053 | biostudies-arrayexpress

S-adenosylmethionine (SAM) changes DNA methylation patterns in prostate cancer cells

2015-03-01 | GSE62053 | GEO

caArray_becic-00235: Gene expression alterations in prostate cancer predicting tumor aggression and preceding development of malignancy

Project description:The incidence of prostate cancer is frequent, occurring in almost one-third of men older than 45 years. Only a fraction of the cases reach the stages displaying clinical significance. Despite the advances in our understanding of prostate carcinogenesis and disease progression, our knowledge of this disease is still fragmented. Identification of the genes and patterns of gene expression will provide a more cohesive picture of prostate cancer biology. PATIENTS AND METHODS: In this study, we performed a comprehensive gene expression analysis on 152 human samples including prostate cancer tissues, prostate tissues adjacent to tumor, and organ donor prostate tissues, obtained from men of various ages, using the Affymetrix (Santa Clara, CA) U95a, U95b, and U95c chip sets (37,777 genes and expression sequence tags). RESULTS: Our results confirm an alteration of gene expression in prostate cancer when comparing with nontumor adjacent prostate tissues. However, our study also indicates that the gene expression pattern in tissues adjacent to cancer is so substantially altered that it resembles a cancer field effect. CONCLUSION: We also found that gene expression patterns can be used to predict the aggressiveness of prostate cancer using a novel model. becic-00235 Assay Type: Gene Expression Provider: Affymetrix Array Designs: HG_U95A, HG_U95Av2, HG_U95B, HG_U95C Organism: Homo sapiens (ncbitax) Material Types: synthetic_RNA, organism_part, whole_organism, total_RNA Disease States: Normal, Prostate_Adenocarcinoma

2015-05-06 | E-GEOD-68555 | biostudies-arrayexpress

caArray_becic-00235: Gene expression alterations in prostate cancer predicting tumor aggression and preceding development of malignancy

2015-05-06 | GSE68555 | GEO

S-Adenosylmethionine treatment diminishes the proliferation of castration- resistant prostate cancer cells by modulating the expression of miRNAs

Project description:AdoMet (S-adenosylmethionine) inhibits cancer cell proliferation and migration via epigenetic alterations. The aim of this study was to investigate whether AdoMet may cause alterations in miRNA expression profiles important for the initiation and progression of prostate cancer. PC-3 cells were treated with AdoMet prior to miRNA sequencing. 17 differentially expressed miRNAs were detected. Target gene prediction was performed by means of databases. Results were aligned to transcriptomic data. Bioinformatic analysis revealed upregulation of anticancerogenic genes, downregulation of cancerogenic-related processes and pathways. Knocking down hsa-miR-192-5p in PC-3 cells resulted in downregulation of cancer cell proliferation, thus confirming these results.

2024-09-10 | E-MTAB-14388 | biostudies-arrayexpress

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