ArticleMolecular oncology2022
The signal transducer CD24 suppresses the germ cell program and promotes an ectodermal rather than mesodermal cell fate in embryonal carcinomas.
Article in Molecular oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 30 citations in OpenAlex.
- Schisantherin A promotes neural differentiation of stem cells from apical papilla to improve mandibular development via mental nerve repair.Stem cell research & therapy · 2026Article
- Phenotype and gene signature of testicular tumors in 129.MOLF-Chr19 mice resemble human teratomas.Andrology · 2025Article
- Induction of SOX17 with stimulation of WNT, TGF-beta, and FGF signaling drives embryonal carcinomas into the yolk-sac tumor lineage resulting in increased cisplatin resistance.International journal of cancer · 2025Article
- Post-Translational Modifications of Proteins Orchestrate All Hallmarks of Cancer.Life (Basel, Switzerland) · 2025Review
- Immune profiling of pediatric germ cell tumors identifies key cell populations and novel therapeutic targets.Frontiers in immunology · 2025Article
- Molecular and histopathological characterization of seminoma patients with highly elevated human chorionic gonadotropin levels in the serum.Virchows Archiv : an international journal of pathology · 2024Article
- Checkpoint CD24 function on tumor and immunotherapy.Frontiers in immunology · 2024Review
- Molecular characterization of the CXCR4 / CXCR7 axis in germ cell tumors and its targetability using nanobody-drug-conjugates.Experimental hematology & oncology · 2023Article
- CD24 targeting with NK-CAR immunotherapy in testis, prostate, renal and (luminal-type) bladder cancer and identification of direct CD24 interaction partners.The FEBS journal · 2023Article
- Targeting CLDN6 in germ cell tumors by an antibody-drug-conjugate and studying therapy resistance of yolk-sac tumors to identify and screen specific therapeutic options.Molecular medicine (Cambridge, Mass.) · 2023Article
- Establishment and Evaluation of Dual HDAC/BET Inhibitors as Therapeutic Options for Germ Cell Tumors and Other Urological Malignancies.Molecular cancer therapeutics · 2022Article
- Profiling the 3D interaction between germ cell tumors and microenvironmental cells at the transcriptome and secretome level.Molecular oncology · 2022Article
- Therapeutical interference with the epigenetic landscape of germ cell tumors: a comparative drug study and new mechanistical insights.Clinical epigenetics · 2022Article
- Expression of CD24 as Cancer Stem Cell Marker in the Diagnosis of Oral Squamous Cell Carcinoma - A Prospective Study.Annals of maxillofacial surgeryArticle
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20 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Testicular germ cell tumors (GCTs) are stratified into seminomas and nonseminomas. Seminomas share many histological and molecular features with primordial germ cells, whereas the nonseminoma stem cell population-embryonal carcinoma (EC)-is pluripotent and thus able to differentiate into cells of all three germ layers (teratomas). Furthermore, ECs are capable of differentiating into extra-embryonic lineages (yolk sac tumors, choriocarcinomas). In this study, we deciphered the molecular and (epi)genetic mechanisms regulating expression of CD24, a highly glycosylated signaling molecule upregulated in many cancers. CD24 is overexpressed in ECs compared with other GCT entities and can be associated with an undifferentiated pluripotent cell fate. We demonstrate that CD24 can be transactivated by the pluripotency factor SOX2, which binds in proximity to the CD24 promoter. In GCTs, CD24 expression is controlled by epigenetic mechanisms, that is, histone acetylation, since CD24 can be induced by the application histone deacetylase inhibitors. Vice versa, CD24 expression is downregulated upon inhibition of histone methyltransferases, E3 ubiquitin ligases, or bromodomain (BRD) proteins. Additionally, three-dimensional (3D) co-cultivation of EC cells with microenvironmental cells, such as fibroblasts, and endothelial or immune cells, reduced CD24 expression, suggesting that crosstalk with the somatic microenvironment influences CD24 expression. In a CRISPR/Cas9 deficiency model, we demonstrate that CD24 fulfills a bivalent role in differentiation via regulation of homeobox, and phospho- and glycoproteins; that is, it is involved in suppressing the germ cell/spermatogenesis program and mesodermal/endodermal differentiation, while poising the cells for ectodermal differentiation. Finally, blocking CD24 by a monoclonal antibody enhanced sensitivity toward cisplatin in EC cells, including cisplatin-resistant subclones, highlighting CD24 as a putative target in combination with cisplatin.
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