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Differential gene and microRNA expression in two SOX2-silenced human embryonal carcinoma cell lines

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

OTHER RELATED OMICS DATASETS IN: E-GEOD-59234PRJNA255220PRJNA255222PRJNA254789

ORGANISM(S): Homo sapiens

PROVIDER: GSE59381 | GEO | 2014/08/15

SECONDARY ACCESSION(S): PRJNA255220

REPOSITORIES: GEO

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Role of SOX2 in the etiology of embryonal carcinoma, based on analysis of the NCCIT and NT2 cell lines.

Project description:The transcription factor SOX2, associated with amongst others OCT3/4, is essential for maintenance of pluripotency and self-renewal of embryonic stem cells. SOX2 is highly expressed in embryonal carcinoma (EC), the stem cell component of malignant nonseminomatous germ cell tumors, referred to as germ cell cancer (GCC). In fact, OCT3/4 together with SOX2 is an informative diagnostic tool for EC in a clinical setting. Several studies support the hypothesis that SOX2 is a relevant oncogenic factor in various cancers and recently, SOX2 has been suggested as a putative therapeutic target for early stage EC. We demonstrate the presence of genomic amplification of SOX2 in an EC cell line, NCCIT, using array comparative genome hybridization and fluorescence in situ hybridization. Down-regulation of SOX2 by targeted siRNA provokes NCCIT cells towards apoptosis, while inhibition of OCT3/4 expression induced differentiation, with retained SOX2 levels. Mice pluripotent xenografts from NCCIT (N-NCCIT and N2-NCCIT) show a consistent SOX2 expression, in spite of loss of the expression of OCT3/4, and differentiation, with retained presence of genomic amplification. No SOX2 amplification has been identified in primary pure and mixed EC in vivo patient samples so far. The data presented in this study are based on a single EC cell line with a SOX2 amplification, with NT2 as control EC cell line, showing no profound induction of apoptosis upon SOX2 downregulation. The findings are of relevance to identify mechanisms involved in the pathogenesis of EC tumors, and support the model of SOX2-oncogene dependency of EC, which however, does not exclude induction of differentiation. This finding is likely related to the presence of wild type p53 in GCC, resulting in expression of downstream target genes, amongst others miR-34a, miR-145 and SOX2, associated to the unique sensitivity of GCC to DNA damaging agents.

| S-EPMC3880257 | biostudies-literature

Gene expression profiles of two lung squamous cell carcinoma cell lines treated with SOX2 siRNA

Project description:SOX2 is a transcription factor essential for self-renewal and pluripotency of embryonic stem cells. Recently SOX2 was found overexpressed in the majority of the lung squamous cell carcinoma (SQC), in which it acts as a lineage-survival oncogene. However, downstream targets/pathways of SOX2 in lung SQC cells remain to be identified. In order to identify genes/pathways likely to be downstream of SOX2, we conducted SOX2 silencing experiments in LK2 and NCI-H520 (H520 thereafter), two SOX2-abundant lung SQC cell lines and analyzed global gene transcription changes by gene expression microarray assay. Each of H520 and LK2 cell lines was treated with either pooled siRNAs of SOX2 or non-silencing (control) siRNAs. After 48 h, cells were harvested and totoal RNA extracted for gene expression microarray analysis using Illumina HumanHT12 v3 BeadChip.

| S-ECPF-GEOD-48871 | biostudies-other

Seminoma and embryonal carcinoma footprints identified by analysis of integrated genome-wide epigenetic and expression profiles of germ cell cancer cell lines

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-01 | E-GEOD-56454 | biostudies-arrayexpress

Molecular consequences of SOD2 expression in epigenetically silenced pancreatic carcinoma cell lines.

Project description:Manganese superoxide dismutase (SOD2) is an enzyme that catalyses the dismutation of superoxide in the mitochondria, leading to reduced levels of reactive oxygen species. Reduced expression levels of SOD2 have been shown to result in increased DNA damage and sod2 heterozygous mice have increased incidences of cancer. It has also been shown that SOD2 expression is lost in pancreatic cell lines, with reintroduction of SOD2 resulting in decreased rate of proliferation. The mechanism of decreased SOD2 expression in pancreatic carcinoma has not been previously determined. We demonstrate, through sodium bisulphite sequencing, that the sod2 locus is methylated in some pancreatic cell lines leading to a corresponding decrease in SOD2 expression. Methylation can be reversed by treatment with zebularine, a methyltransferase inhibitor, resulting in restored SOD2 expression. Furthermore, we demonstrate that sensitivity of pancreatic carcinoma cell lines to 2-methoxyestradiol correlates with SOD2 expression and SOD2 modulation can alter the sensitivity of these cells. Using both genomics and proteomics, we also identify molecular consequences of SOD2 expression in MIA-PaCa2 cells, including dephosphorylation of VEGFR2 and the identification of both SOD2-regulated genes and transcription factors with altered binding activity in response to SOD2 expression.

| S-EPMC2360443 | biostudies-literature

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.

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.

2014-08-15 | GSE59380 | GEO

Seminoma and embryonal carcinoma footprints identified by analysis of integrated genome-wide epigenetic and expression profiles of germ cell cancer cell lines

Project description:This SuperSeries is composed of the SubSeries listed below.

2014-06-01 | GSE56454 | GEO

Acute hypersensitivity of pluripotent testicular cancer-derived embryonal carcinoma to low-dose 5-aza deoxycytidine

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2012-12-01 | E-GEOD-42647 | biostudies-arrayexpress

Differential expression analysis of colorectal carcinoma cells (D53wt)

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-02-04 | E-GEOD-43914 | biostudies-arrayexpress

SOX2 is essential for in vivo reprogramming of seminoma-like TCam-2 cells to an embryonal carcinoma-like fate.

Project description:Type II germ cell cancers (GCC) are divided into seminomas, which are highly similar to primordial germ cells and embryonal carcinomas (EC), often described as malignant counterparts to embryonic stem cells.Previously, we demonstrated that the development of GCCs is a highly plastic process and strongly influenced by the microenvironment. While orthotopic transplantation into the testis promotes seminomatous growth of the seminoma-like cell line TCam-2, ectopic xenotransplantation into the flank initiates reprogramming into an EC-like fate.During this reprogramming, BMP signaling is inhibited, leading to induction of NODAL signaling, upregulation of pluripotency factors and downregulation of seminoma markers, like SOX17. The pluripotency factor and EC-marker SOX2 is strongly induced.Here, we adressed the molecular role of SOX2 in this reprogramming. Using CRISPR/Cas9-mediated genome-editing, we established SOX2-deficient TCam-2 cells. Xenografting of SOX2-deficient cells into the flank of nude mice resulted in maintenance of a seminoma-like fate, indicated by the histology and expression of OCT3/4, SOX17, TFAP2C, PRDM1 and PRAME. In SOX2-deficient cells, BMP signaling is inhibited, but NODAL signaling is not activated. Thus, SOX2 appears to be downstream of BMP signaling but upstream of NODAL activation. So, SOX2 is an essential factor in acquiring an EC-like cell fate from seminomas.A small population of differentiated cells was identified resembling a mixed non-seminoma. Analyses of these cells revealed downregulation of the pluripotency and seminoma markers OCT3/4, SOX17, PRDM1 and TFAP2C. In contrast, the pioneer factor FOXA2 and its target genes were upregulated, suggesting that FOXA2 might play an important role in induction of non-seminomatous differentiation.

| S-EPMC5216926 | biostudies-literature

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