PXD025110

PXD025110 is an original dataset announced via ProteomeXchange.

Title	Molecular and epigenetic characterization of the signal transducer CD24 in germ cell tumors
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).
HostingRepository	PRIDE
AnnounceDate	2022-01-19
AnnouncementXML	Submission_2022-01-19_02:55:03.731.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	Anja Stefanski
SpeciesList	scientific name: Homo sapiens (Human); NCBI TaxID: 9606;
ModificationList	iodoacetamide derivatized residue
Instrument	Q Exactive

Revision	Datetime	Status	ChangeLog Entry
0	2021-03-30 10:43:16	ID requested
⏵ 1	2022-01-19 02:55:04	announced

Skowron MA, Becker TK, Kurz L, Jostes S, Bremmer F, Fronhoffs F, Funke K, Wakileh GA, M, ü, ller MR, Burmeister A, Lenz T, Stefanski A, St, ü, hler K, Petzsch P, K, ö, hrer K, Altevogt P, Albers P, Kristiansen G, Schorle H, Nettersheim D, The signal transducer CD24 suppresses the germ cell program and promotes an ectodermal rather than mesodermal cell fate in embryonal carcinomas. Mol Oncol, 16(4):982-1008(2022) [pubmed]

submitter keyword: CD24, germ cell tumors, embryonal carcinoma, differentiation, pluripotency, epigenetics

Kai Stühler
contact affiliation	Institute for Molecular Medicine, Heinrich-Heine-University, Med. Faculty, Düsseldorf, Germany; Molecular Proteomics Laboratory, Centre for Biological and Medical Research (BMFZ), Heinrich-Heine-University, Düsseldorf, Germany.
contact email	Daniel.Nettersheim@med.uni-duesseldorf.de
lab head
Anja Stefanski
contact affiliation	Molecular Proteomics Laboratory
contact email	anja.stefanski@hhu.de
dataset submitter

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PRIDE project URI

• PRIDE
  1. PXD025110
     1. Label: PRIDE project
     2. Name: Molecular and epigenetic characterization of the signal transducer CD24 in germ cell tumors