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ChIP-seq. analysis of pan-histone 3 acetylation in Romidepsin treated TCam-2

ABSTRACT: ChIP-seq. analysis of TCam-2 16 h after 10 nanomolar Romidepsin application. DMSO treated cells were used as controls. For ChIP, an antibody against histone H3 pan-acetylation was used. These data are part of the article 'The Histone Deacetylase Inhibitor Romidepsin Efficiently Targets Cisplatin-resistant Germ Cell Cancer Cells via Downregulation of the SWI/SNF-Complex Member ARID1A' (Nettersheim et al., 2016).

ORGANISM(S): Homo sapiens

PROVIDER: GSE78262 | GEO | 2016/09/01

SECONDARY ACCESSION(S): PRJNA313057

REPOSITORIES: GEO

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ChIP-seq. analysis of pan-histone 3 acetylation in Romidepsin treated TCam-2

Project description:ChIP-seq. analysis of TCam-2 16 h after 10 nanomolar Romidepsin application. DMSO treated cells were used as controls. For ChIP, an antibody against histone H3 pan-acetylation was used. These data are part of the article 'The Histone Deacetylase Inhibitor Romidepsin Efficiently Targets Cisplatin-resistant Germ Cell Cancer Cells via Downregulation of the SWI/SNF-Complex Member ARID1A' (Nettersheim et al., 2016). TCam-2 cells treated for 16h with romidepsin or the solvent were fixed by formaldehyde solution and further processed by Active Motif, including DNA shearing by sonication, chromatin-immunoprecipitaion, library generation and sequencing (NextSeq 500, Illumina). Pooled input DNA of each sample including spike-in Drosophila DNA was used as controls and for normalization. The 75-nt sequence reads were mapped against the genome using BWA algorithm. Duplicate reads were removed. Only peaks that align with no more than 2 mismatches and map uniquely to the genome were used for further analysis. Intervals / peaks were identified by the MACS peak finding algorithm (cutoff p-value 1x10-7) including ENCODE blacklist filtering

2016-09-01 | E-GEOD-78262 | biostudies-arrayexpress

Genome-wide expression microarray analysis of romidpesin treated GCC cell lines, fibroblasts and Sertoli cells.

Project description:Illumina expression microarray analysis of TCam-2, 2102EP, NCCIT, JAR, MPAF, ARZ and FS1 cells 8 and 16 h after 10 nanomolar romidepsin application. DMSO treated cells were used as controls. These data are part of the article 'A signaling cascade including ARID1A, GADD45B and DUSP1 induces apoptosis and affects the cell cycle of germ cell cancers after romidepsin treatment' (Nettersheim et al., 2016).

2016-09-23 | GSE71239 | GEO

Genome-wide DNA methylation analysis of Romidpesin treated GCC cell lines

Project description:Illumina 450k DNA methylation microarray analysis of TCam-2, 2102EP, NCCIT and JAR cells 16 h after 10 nanomolar Romidepsin application. DMSO treated cells were used as controls. These data are part of the article 'The Histone Deacetylase Inhibitor Romidepsin is a Novel Therapeutic Option for (Cisplatin-resistant) Germ Cell Cancers' (Nettersheim et al., 2016).

2016-05-01 | GSE76709 | GEO

Genome-wide DNA methylation analysis of seminoma-like TCam-2 cells during transition into an embryonal carcinoma-like state

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Genome-wide expression microarray analysis of seminoma-like TCam-2 cells during transition into an embryonal carcinoma-like state

Project description:Illumina expression microarray analysis of seminoma-like TCam-2 cells xenografted in nude mice. 2120EP embryonal carcinoma cells served as control. TCam-2 cells acquire pluripotency and become epigenetically reprogrammed to an embryonal carcinoma-like state during in vivo growth. This analysis is part of the article 'BMP inhibition in seminomas initiates acquisition of pluripotency via NODAL signaling resulting in reprogramming to an embryonal carcinoma' by Nettersheim et al., 2015. PLoS Genetics

2015-08-01 | GSE60698 | GEO

Genome-wide DNA methylation analysis of seminoma-like TCam-2 cells during transition into an embryonal carcinoma-like state

Project description:Illumina 450k DNA methylation microarray analysis of seminoma-like TCam-2 cells xenografted in nude mice. 2120EP embryonal carcinoma cells served as control. TCam-2 cells acquire pluripotency and become epigenetically reprogrammed to an embryonal carcinoma-like state during in vivo growth. This analysis is part of the article 'BMP inhibition in seminomas initiates acquisition of pluripotency via NODAL signaling resulting in reprogramming to an embryonal carcinoma' by Nettersheim et al., 2015. PLoS Genetics Genomic DNA was isolated from tumors of TCam-2 and 2102EP cells xenografted for 1, 2, 4 and 6 weeks as well as 4 and 8 weeks, respectively. In vivo samples of TCam-2 cells were analyzed in biological duplicates. In vitro cultivated TCam-2 / 2102EP cells as well as 2102EP xenografted for 4 and 8 weeks were analyzed once.

2015-08-01 | E-GEOD-60787 | biostudies-arrayexpress

Genome-wide cDNA expression analysis of seminoma-like TCam-2 cells during transition into an embryonal carcinoma-like state

Project description:Illumina cDNA expression microarray analysis of seminoma-like TCam-2 cells xenografted in nude mice. 2120EP embryonal carcinoma cells served as control. TCam-2 cells acquire pluripotency and become epigenetically reprogrammed to an embryonal carcinoma-like state during in vivo growth. This analysis is part of the article 'BMP inhibition in seminomas initiates acquisition of pluripotency via NODAL signaling resulting in reprogramming to an embryonal carcinoma' by Nettersheim et al., 2015. PLoS Genetics Total RNA was isolated from tumors of TCam-2 and 2102EP cells xenografted for 1, 2, 4 and 6 weeks as well as 4 and 8 weeks, respectively. 1x10^7 cells were xenografted. In vivo samples of TCam-2 cells were analyzed in biological duplicates. In vitro cultivated TCam-2 / 2102EP cells as well as 2102EP xenografted for 4 and 8 weeks were analyzed once.

2015-08-01 | E-GEOD-60698 | biostudies-arrayexpress

Genome-wide expression microarray analysis of SOX2-deficient TCam-2 cells in vivo

Project description:Illumina expression microarray analysis of seminoma-like TCam-2 cells depleted for SOX2 by CRISPR/Cas9. Cells were xenografted in nude mice. 2120EP embryonal carcinoma and parental TCam-2 cells were xenograted as controls. Tumors were recovered after 1 (1w) and 6 weeks (clone 1 - 5) of in vivo growth. Additionally, in vitro cultivated TCam-2 were analyzed as control. The data set is part of the study 'SOX2 is essential for in vivo reprogramming of seminoma-like TCam-2 cells to an embryonal carcinoma-like fate' (Nettersheim et al., 2016, Oncotarget).

2016-05-22 | GSE79065 | GEO

Genome-wide expression microarray analysis of PRAME knock down TCam-2 cells with and without ATRA treatment

Project description:Illumina expression microarray analysis of shRNA-mediated PRAME knock down TCam-2 cells with and without all trans retinoic acid (ATRA) treatment for 8 days, of TCam-2 cells with and without ATRA (8d) and of in vitro cultivated GCC cell lines TCam-2, 2102EP, NCCIT and JAR. These data are part of the article 'The Cancer / Testis-Antigen PRAME supports the pluripotency network and represses somatic and germ cell differentiation programs in seminomas'.

2016-05-22 | GSE71269 | GEO

Expression data of Panc1 cells treated with romidepsin and tamoxifen

Project description:Tamoxifen enhances romidepsin-induced senescence in pancreatic cancer cells. We compared gene-expression profile among untreated control, romidepsin-treated, tamoxifen-treated, and romidepsin plus tamoxifen-treated Panc1 cells.

2021-08-21 | GSE182526 | GEO

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