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E-GEOD-59234

ABSTRACT: Gene expression data from SOX2 knock-out 2102Ep and NTera-2 human embryonal carcinoma cell lines

OTHER RELATED OMICS DATASETS IN: GSE59381PRJNA255220PRJNA255222PRJNA254789

PROVIDER: E-GEOD-59234 | ExpressionAtlas | 2014-09-05

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-59234-analysis-methods.tsv	Tabular
	E-GEOD-59234-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-59234-configuration.xml	Xml
	E-GEOD-59234-percentile-ranks.tsv	Tabular
	E-GEOD-59234.condensed-sdrf.tsv	Tabular

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Gene expression data from SOX2 knock-out 2102Ep and NTera-2 human embryonal carcinoma cell lines

Project description:SOX2 is an oncogene and a core pluripotency transcription factor. SOX2 has multiple roles in various malignancies, in the maintainance of pluripotency and during various stages of embryonic development. Human embryonal carcinoma cells express SOX2 and the loss of this results in their differentiation. We silenced SOX2 in two human embryonal carcinoma cell lines and measured whole-genome mRNA expression. Many genes related to embryogenesis and tissue morphogensis were upregulated. Other upregulated genes were markers of mesodermal development and epithelial-to-mesenchymal transition. A specific and validated siRNA against SOX2 was chemically transfected in undifferentiated 2102Ep and NTera-2 embryonal carcinoma cell lines. After three days of incubation under normal growth conditions we used Affymetrix microarrays to measure whole-genome mRNA transcript expression in three biological replicates of each cell line and compared this to whole-gene expression in identical samples transfected with a non-targeting, scrambled control siRNA. SOX2 silencing was validated using qRT-PCR and Western blot prior to whole-genome expression analysis.

2014-08-15 | E-GEOD-59234 | biostudies-arrayexpress

FSCN1 as a new druggable target in adrenocortical carcinoma

Project description:Adrenocortical carcinoma (ACC) is a rare endocrine malignancy with a high risk of relapse and metastatisation. The actin-bundling protein fascin (FSCN1) is overexpressed in aggressive ACC and represents a reliable prognostic indicator. FSCN1 has been shown to synergize with the Rho/Rac GEF VAV2 in enhancing the invasion properties of ACC cancer cells. Based on those results, we investigated the effects of FSCN1 inactivation by CRISPR/Cas9 or pharmacological blockade on the invasive properties of ACC cells, both in vitro and in an in vivo metastatic ACC zebrafish model. Here we showed that FSCN1 is a transcriptional target for Beta-catenin in H295R ACC cells and that its inactivation resulted in defects in cell attachment and proliferation. Additionally, FSCN1 knock-out modulated the expression of genes involved in cytoskeleton dynamics and cell adhesion. When SF-1 dosage was upregulated in H95R cells, activating their invasive capacities, FSCN1 knock-out reduced the number of filopodia, lamellipodia/ruffles and focal adhesions, while decreasing cell invasion in Matrigel. Similar effects were produced by the FSCN1 inhibitor G2-044, which also diminished the invasion of ACC cell lines (CU-ACC2, JIL-2266, MUC-1) expressing lower levels of FSCN1 than H295R. In the zebrafish model, metastases formation was significantly reduced in FSCN1 knock-out cells and G2-044 significantly reduced the number of metastases formed by ACC cells. Our results indicate that FSCN1 represents a new druggable target for ACC and provide the rationale for future clinical trials with FSCN1 inhibitors in patients with ACC, possibly in combination with immunotherapy.

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Gene expression data from SOX2 knock-out 2102Ep and NTera-2 human embryonal carcinoma cell lines

2014-08-15 | GSE59234 | GEO

MiRNA expression data from SOX2 knock-out 2102Ep and NTera-2 human embryonal carcinoma cell lines

Project description:SOX2 is an oncogene and a core pluripotency transcription factor. SOX2 has multiple roles in various malignancies, in the maintenance of pluripotency and during various stages of embryonic development. Human embryonal carcinoma cells express SOX2 and the loss of this results in their differentiation. We silenced SOX2 in two human embryonal carcinoma cell lines and measured the differential expression of 754 unique mature miRNAs. This revealed the deregulation of many oncomiRs, tumour suppressor miRNAs and developmental miRNAs, including those belonging to the C19MC cluster.

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