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RNA sequencing data of NCCIT cells deficient for CD24 and parental controls

ABSTRACT: RNA sequencing data of NCCIT cells deficient for CD24 and parental controls

PROVIDER: PRJNA713323 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13927047.fastq.gz	Fastqsanger.gz
	SRR13927048.fastq.gz	Fastqsanger.gz
	SRR13927049.fastq.gz	Fastqsanger.gz
	SRR13927050.fastq.gz	Fastqsanger.gz
	SRR13927051.fastq.gz	Fastqsanger.gz

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RNA sequencing data of NCCIT cells deficient for CD24 and parental controls

Project description:Single eng 3' RNA sequencing of embryonal carcinoma cell line NCCIT deficient for CD24 and parental cells. CD24 deficiency was genereted by CRISPR/Cas9 method. Five different NCCIT knock out clones were sequenced.

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Illumina Infinium MethylationEPIC BeadChip (850k) data of NCCIT / 2102EP cells deficient for CD24 and parental controls

Project description:Illumina Infinium MethylationEPIC BeadChip (850k) array analysis of DNA methylation of embryonal carcinoma cell lines NCCIT and 2102EP deficient for CD24 and parental cells. CD24 deficiency was genereted by CRISPR/Cas9 method. Three different NCCIT and 2102EP knock out clones were analyzed.

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Illumina Infinium MethylationEPIC BeadChip (850k) data of NCCIT / 2102EP cells deficient for CD24 and parental controls

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Project description:Being involved in adhesion, migration, and invasion, the highly glycosylated signal transducer CD24 (cluster of differentiation 24) has been implicated to play an essential role during carcinogenesis. Previously, the molecular and (epi)genetic regulation of CD24 has been characterized in testicular germ cell tumors (GCT). Here, CD24 was exclusively found in embryonal carcinoma (EC), which represents the stem cell like population of GCT (see project PXD025110). For a better understanding of the molecular function of CD24, this study aimed at the identification of the direct interaction partners of CD24 not only in GCTs, but also in other urologic malignancies, such as urothelial- (UC), prostate- (PC), and renal cell carcinoma (RCC). For this purpose, co-immunoprecipitations of CD24 were performed in GCT, UC, PC, and RCC cell lines, while CD24-deficient EC cells as well as IgG2a controls were included for high validity. Extracted proteome was measured by liquid-chromatography coupled with mass spectrometry (LS-MS).

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Molecular and epigenetic characterization of the signal transducer CD24 in germ cell tumors

Project description:Type II germ cell tumors (GCTs) are with more than 90% 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. The non-seminomatous stem-cell like embryonal carcinomas (EC) can further differentiate into teratomas (TE), yolk sac tumors (YST), or choriocarcinomas (CC). Orchiectomy followed by chemo- or radiotherapy is a widely used procedure in the treatment of type II GCTs, leading to high cure rates of up to 90%. Nevertheless, about 10 - 15% of patients with progressive disease relapse as a result of drug resistance and are condemned for a poor prognosis and a short survival of only a few months. Cluster of differentiation 24 (CD24) is a small, mucin-like glycosylphosphatidylinositol (GPI) anchored membrane molecule that functions both, in signal transduction and as an adhesion molecule. This glycoprotein is mainly expressed on the surface of hematopoietic, neural, muscular, and epithelial cells. Moreover, CD24 has been implicated in tumor metastasis, as fucosylated CD24 interacts with P- and E-selectin, allowing invasion of tumor cells to distal sites. High expression or amplifications of CD24 has been described in a variety of solid malignancies, such as non-small cell lung carcinoma, gliomas, breast cancer, retinoblastoma, hepatocellular carcinoma, renal cell carcinoma, cervical carcinoma, prostate cancer, urothelial carcinoma, pineal parenchymal tumors, and ovarian cancer. In this study, we investigated the putative function of CD24 and its interaction partners in (cisplatin-resistant) GCT cell lines by generating CD24-deficient EC cells by CRISPR/Cas9-mediated gene editing. Changes in the proteome between CD24-deficient cells and parental cells were measured by liquid-chromatography coupled with mass spectrometry (LS-MS).

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