ArticleOncogene2005
Aberrant NF-kappaB2/p52 expression in Hodgkin/Reed-Sternberg cells and CD30-transformed rat fibroblasts.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- The non-canonical NF-κB pathway in immunity and inflammation.Nature reviews. Immunology · 2017Review
- NF-κB in Hematological Malignancies.Biomedicines · 2017Review
- NF-κB signaling pathway and its potential as a target for therapy in lymphoid neoplasms.Blood reviews · 2017Review
- TRAF2 recruitment via T61 in CD30 drives NFκB activation and enhances hESC survival and proliferation.Molecular biology of the cell · 2015Article
- Mechanisms and consequences of constitutive NF-κB activation in B-cell lymphoid malignancies.Oncogene · 2014Review
- NF-κB pathways in hematological malignancies.Cellular and molecular life sciences : CMLS · 2014Review
- Article
- Notch is an essential upstream regulator of NF-κB and is relevant for survival of Hodgkin and Reed-Sternberg cells.Leukemia · 2012Article
- Article
- Non-canonical NF-κB signaling pathway.Cell research · 2011Review
- CD30-induced signaling is absent in Hodgkin's cells but present in anaplastic large cell lymphoma cells.The American journal of pathology · 2008Article
- hESC adaptation, selection and stability.Stem cell reviews · 2007Review
- Stat3 activation of NF-{kappa}B p100 processing involves CBP/p300-mediated acetylation.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- cIAP2 is highly expressed in Hodgkin-Reed-Sternberg cells and inhibits apoptosis by interfering with constitutively active caspase-3.Journal of molecular medicine (Berlin, Germany) · 2006Article
- Review
- Hodgkin's lymphoma cells are efficiently engrafted and tumor marker CD30 is expressed with constitutive nuclear factor-kappaB activity in unconditioned NOD/SCID/gammac(null) mice.Cancer science · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of CD30 and constitutive nuclear factor-kappaB (NF-kappaB) activation are hallmarks of the malignant Hodgkin Reed-Sternberg (H-RS) cells. Previous investigations have demonstrated that both proliferation and survival of H-RS cells require constitutive NF-kappaB activity, which is comprised of the p50 and RelA subunits. We report here enhanced expression of NF-kappaB2/p52 and RelB-containing NF-kappaB DNA-binding activity in Epstein-Barr virus-negative H-RS cells. Kinetic studies revealed that a proteasome inhibitor MG132 induced p100 accumulation with reduced p52 expression in H-RS cells, suggesting proteasome-dependent processing of p100. In addition, treatment with a protein synthesis inhibitor cycloheximide rapidly downregulated inhibitor of NF-kappaB (IkappaB) kinase activity in H-RS cells. We also demonstrate that overexpression of CD30 in rat fibroblasts at levels comparable to those in H-RS cells results in constitutive IkappaB kinase activation, proteasome-dependent p100 processing, and NF-kappaB-dependent cell transformation. Our results thus indicate that CD30 triggers the noncanonical NF-kappaB activation pathway, and suggest that deregulated CD30 signaling contributes to the neoplastic features of H-RS cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.