ArticleThe American journal of pathology2003
AP-1 mediated relief of repressive activity of the CD30 promoter microsatellite in Hodgkin and Reed-Sternberg cells.
Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 51 citations in OpenAlex.
- CRISPR Screens Reveal Epstein-Barr Virus-activated JunB as a Key Lymphoblastoid B cell Dependency Factor that Represses Cyclin Dependent Kinase Inhibitor P18INK4c.bioRxiv : the preprint server for biology · 2026Article
- CD30 as a Target Molecule in the Diagnosis and Therapy of Lymphomas.American journal of hematology · 2026Review
- CAR-T Cell Therapy for Classical Hodgkin Lymphoma.HemaSphere · 2023Review
- CD30 stimulation induces multinucleation and chromosomal instability in HTLV-1-infected cell lines.International journal of hematology · 2023Article
- CD30 Expression and Its Functions during the Disease Progression of Adult T-Cell Leukemia/Lymphoma.International journal of molecular sciences · 2023Review
- Mechanism of action and therapeutic targeting of CD30 molecule in lymphomas.Frontiers in oncology · 2023Review
- Super-enhancer-based identification of a BATF3/IL-2R-module reveals vulnerabilities in anaplastic large cell lymphoma.Nature communications · 2021Article
- Molecular biology of Hodgkin lymphoma.Leukemia · 2021Review
- AP-1 family transcription factors: a diverse family of proteins that regulate varied cellular activities in classical hodgkin lymphoma and ALK+ ALCL.Experimental hematology & oncology · 2021Review
- The c-Jun and JunB transcription factors facilitate the transit of classical Hodgkin lymphoma tumour cells through GScientific reports · 2018Article
- Human CD30+ B cells represent a unique subset related to Hodgkin lymphoma cells.The Journal of clinical investigation · 2018Article
- Review
- Article
- Understanding CD30 biology and therapeutic targeting: a historical perspective providing insight into future directions.Blood cancer journal · 2017Review
- Expression patterns of the activator protein-1 (AP-1) family members in lymphoid neoplasms.Clinical and experimental medicine · 2017Review
- Mapping of transcription factor motifs in active chromatin identifies IRF5 as key regulator in classical Hodgkin lymphoma.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Cleavage of the JunB transcription factor by caspases generates a carboxyl-terminal fragment that inhibits activator protein-1 transcriptional activity.The Journal of biological chemistry · 2013Article
- Ets-1 activates overexpression of JunB and CD30 in Hodgkin's lymphoma and anaplastic large-cell lymphoma.The American journal of pathology · 2012Article
- The biology of Hodgkin's lymphoma.Nature reviews. Cancer · 2009Review
- JunB expression is a common feature of CD30+ lymphomas and lymphomatoid papulosis.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2005Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of CD30 is the hallmark of Hodgkin and Reed-Sternberg (H-RS) cells and drives constitutive nuclear factor-kappaB activation that is the molecular basis for the pathophysiology of Hodgkin's lymphoma. Transcription of the CD30 gene is controlled by the core promoter that is driven by Sp-1 and the microsatellite sequences (MSs) that represses core promoter activity. To understand the mechanism(s) of CD30 overexpression in H-RS cells, we structurally and functionally characterized the CD30 MSs. Although the CD30 MS of H-RS cell lines was polymorphic, it was not truncated compared with that of control cells. A strong core promoter activity and constitutive Sp-1 binding were revealed in all cell lines examined irrespective of the levels of CD30 expression. In transient reporter gene assays, all MS clones derived from H-RS cell lines repressed the core promoter activity in unrelated cell lines, but not in the H-RS cell lines. An AP-1-binding site was found in the MS at nucleotide position of -377 to -371, the presence of which was found to relieve repression of the core promoter in H-RS cell lines but not in other tumor cell lines. H-RS cell lines showed constitutive and strong AP-1-binding activity, but other cell lines did not. The AP-1 complex contained JunB, whose overexpression activated reporter constructs driven by the CD30 promoter including the MSs, and was dependent on the AP-1 site. JunB expression was detected in H-RS cells in vitro and in vivo, but not in reactive cells or tumor cells of non-Hodgkin's lymphoma of diffuse large B-cell type. Transduction of JunB small interfering RNAs suppressed CD30 promoter activity in L428 cells but not in control cells. Taken together, overexpression and binding of JunB to the AP-1 site appear to relieve the repression of the core promoter by the CD30 MS in H-RS cells, which provide one basis for the constitutive overexpression of CD30 in Hodgkin's lymphoma.
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