ArticleCancer letters2011
A rearranged EP300 gene in the human B-cell lymphoma cell line RC-K8 encodes a disabled transcriptional co-activator that contributes to cell growth and oncogenicity.
Article in Cancer letters, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Genome-wide CRISPR screens reveal synthetic lethal interaction between CREBBP and EP300 in diffuse large B-cell lymphoma.Cell death & disease · 2021Article
- Sea anemone model has a single Toll-like receptor that can function in pathogen detection, NF-κB signal transduction, and development.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Evidence for an oncogenic modifier role for mutant histone acetyltransferases in diffuse large B-cell lymphoma.Leukemia & lymphoma · 2016Article
- Histone acetyltransferases and histone deacetylases in B- and T-cell development, physiology and malignancy.Genes & cancer · 2015Review
- c-Rel regulates Ezh2 expression in activated lymphocytes and malignant lymphoid cells.The Journal of biological chemistry · 2014Article
- Histone acetyltransferase-deficient p300 mutants in diffuse large B cell lymphoma have altered transcriptional regulatory activities and are required for optimal cell growth.Molecular cancer · 2014Article
- Article
- Epigenetics and B-cell lymphoma.Current opinion in hematology · 2011Review
- The c-Rel Transcription Factor in Development and Disease.Genes & cancer · 2011Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Human diffuse large B-cell lymphoma cell line RC-K8 has an altered EP300 locus that encodes a C-terminally truncated histone acetyltransferase (HAT) protein (p300ΔC). We now show that p300ΔC contains 1047N-terminal amino acids of p300 fused to 25 amino acids encoded by sequences from chromosome 6. Over-expressed p300ΔC localized to nuclear subdomains and interacted with transcription factor REL. p300ΔC did not function as a co-activator for REL-directed transactivation, and blocked the ability of wild-type p300 to enhance transcriptional activation by REL. Knock down of p300ΔC in RC-K8 cells reduced their growth in both liquid culture and soft agar. Truncations of p300 were not found in eight other B-lymphoma cell lines. These results suggest that p300ΔC contributes to the oncogenic state of RC-K8 cells by acting as a defective co-activator.
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