Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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'.

ORGANISM(S): Homo sapiens

PROVIDER: GSE71269 | GEO | 2016/05/22

SECONDARY ACCESSION(S): PRJNA290731

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA sequencing data of TCam-2, 2102EP, JAR, JEG-3, NCCIT, and MPAF fibroblast cells treated with palbociblic and H2O pH3 as solvent control

Project description:RNA sequencing data of TCam-2, 2102EP, JAR, JEG-3, NCCIT, and MPAF fibroblast cells treated with palbociblic and H2O pH3 as solvent control

2021-12-15 | GSE190792 | 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 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 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 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

Identification of factors secreted by testicular germ cell tumor cell lines and microenvironmental cells.

Project description:Type II germ cell tumors (GCTs) are the most common neoplasia in young men of age 14-45 years. It is generally accepted that GCTs arise from a common precursor lesion, called germ cell neoplasia in situ (GCNIS), eventually developing into seminomas or non-seminomas, such as (embryonal carcinomas, ECs). The latter stem-cell like EC can further differentiate into teratomas (TE), yolk-sac tumors (YST), or choriocarcinomas (CC). Even though cisplatin-based chemotherapy is an efficacious standard of care during the management of GCT patients, the development of cisplatin resistance remains a major obstacle. As such, the surrounding tumor microenvironment and its secreted factors could endorse the development of drug resistance. These stromal cells, including immune cells (e.g. macrophages, T-lymphocytes), endothelial cells, and fibroblasts, can influence tumor cells by promoting proliferative and anti-apoptotic signaling pathways. Vice versa, microenvironmental cells can be influenced by tumor cells as well. For the identification of secreted proteins, cell lysates and supernatants from seven human germ cell tumor cell lines (seminoma: TCam-2; embryonal carcinoma (EC): 2102EP, NCCIT; choriocarcinoma (CC): JAR, JEG-3), yolk-sac tumor (YST): GCT72; 1411H) and five human cell types from the microenvironment (fibroblasts: MPAF, HVHF2; M2 macrophages: THP-1-M2; T-lymphocytes: JURKAT; endothelial cells: HUVEC) have been evaluated using liquid chromatography coupled with mass spectrometry (LC-MS).

2022-10-13 | PXD031329 | Pride

RNA sequencing data of germ cell tumor cell lines co-cultured with microenvironmental cells in 3D

Project description:Single end 3' RNA sequencing of GFP-transduced germ cell tumor cell lines (TCam-2, 2102EP, JAR, GCT72) co-cultured in 3D with mCherry-transduced or deepred-stained microenvironmental cells (HUVEC, JURKAT, THP-1-M2, HVHF2) for 72 h before cell sorting both populations using flow cytometry.

2022-04-01 | GSE195794 | GEO

Transcriptional CDK inhibitors as potential treatment option for testicular germ cell tumors

Project description:Type II testicular germ cell tumors (TGCT) are the most frequently diagnosed solid malignancy in young men. Up to 15 % of patients with metastatic non-seminomas show cisplatin resistance having a very poor survival rate due to lacking treatment options. Transcriptional cyclin-dependent kinases (CDK) have been shown to be effective targets in treatment of different types of cancer. Here, we investigated the effects of the CDK inhibitors dinaciclib, flavopiridol, YKL-5-124, THZ1, NVP2, SY0351 and THZ531. XTT viability assay revealed strong cytotoxic impact of CDK7/ 12/ 13 inhibitor SY0351 and CDK9 inhibitor NVP2 on the TGCT wild type cell lines (2102EP, NCCIT, TCam2) and the cisplatin resistant cell lines (2102EP-R, NCCIT-R). The CDK7 inhibitor YKL-5-124 showed strong impact on 2102EP, 2102EP-R, NCCIT and NCCIT-R cell lines leaving the MPAF control cell line mostly unaffected. FACS based analysis revealed mild effects on the cell cycle of 2102EP and TCam2 cells after SY0351, YKL-5-124 or NVP2 treatment. Molecular analysis showed a cell line specific response for SY0351 and NVP2 inhibition while YKL-5-124 induced similar molecular changes in 2102EP, TCam2 and MPAF cells. Thus, after TGCT subtype determination CDK inhibitors might be a potential alternative for optimized and individualized therapy independent of chemotherapy sensitivity.

2022-03-26 | GSE198248 | GEO

PRAME induced inhibition of retinoic acid receptor signaling-mediated differentiation - a possible target for ATRA response in AML without t(15;17)

2013-03-10 | GSE43258 | GEO

PRAME induced inhibition of retinoic acid receptor signaling-mediated differentiation - a possible target for ATRA response in AML without t(15;17)

Project description:Purpose: In acute myeloid leukemia (AML) without retinoic acid receptor (RAR) rearrangement the effect of all-trans retinoic acid (ATRA) is still poorly understood despite an association of NPM1 mutation and ATRA response. Recently, PRAME (preferentially expressed antigen in melanoma) has been shown to be a dominant repressor of RAR-signaling. Experimental design: Thus, we further investigated ATRA response mechanisms, especially the impact of PRAME expression on ATRA-responsiveness by profiling gene expression in K562 cell lines. Results: Our data revealed a PRAME-expression associated gene pattern to be significantly enriched for genes involved in the retinoic acid metabolic process. In leukemia cell line models we could demonstrate that retinoic acid-regulated cell proliferation and differentiation are impacted by PRAME expression. Conclusions: PRAME seems to impair differentiation and to increase proliferation likely via blocking RAR-signaling, which might be reversed by ATRA. For the cell line model GEP was performed using Affymetrix Human Genome U133plus2.0 Array technology according to the manufacturerM-bM-^@M-^Ys recommendations as previously reported. siRNA and scrRNA treated as well as ATRA treated K562 cells stemming from independent experiments were profiled. Using the BRB Array Tools software package fluorescence ratios were normalized by applying the RMA algorithm and supervised ClassComparison PathwayClassComparison analyses were performed.

2013-03-10 | E-GEOD-43258 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data