ArticleOncogene2013
Recruitment of the tumour suppressor protein p73 by Kaposi's Sarcoma Herpesvirus latent nuclear antigen contributes to the survival of primary effusion lymphoma cells.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Kaposi's sarcoma-associated herpesvirus terminal repeat regulates inducible lytic gene promoters.Journal of virology · 2024Article
- The Impact of Co-Infections for Human Gammaherpesvirus Infection and Associated Pathologies.International journal of molecular sciences · 2023Review
- KSHV LANA acetylation-selective acidic domain reader sequence mediates virus persistence.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Regulating tumor suppressor genes: post-translational modifications.Signal transduction and targeted therapy · 2020Review
- The interplay between Epstein-Bar virus (EBV) with the p53 and its homologs during EBV associated malignancies.Heliyon · 2019Review
- Review
- Gene essentiality landscape and druggable oncogenic dependencies in herpesviral primary effusion lymphoma.Nature communications · 2018Article
- Kaposi sarcoma herpesvirus pathogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Effects of the NEDD8-Activating Enzyme Inhibitor MLN4924 on Lytic Reactivation of Kaposi's Sarcoma-Associated Herpesvirus.Journal of virology · 2017Article
- Kaposi's sarcoma-associated herpesvirus stably clusters its genomes across generations to maintain itself extrachromosomally.The Journal of cell biology · 2017Article
- Antimicrobial sulfonamides clear latent Kaposi sarcoma herpesvirus infection and impair MDM2-p53 complex formation.The Journal of antibiotics · 2017Article
- SIRT1 and AMPK pathways are essential for the proliferation and survival of primary effusion lymphoma cells.The Journal of pathology · 2017Article
- Article
- Regulation of the Abundance of Kaposi's Sarcoma-Associated Herpesvirus ORF50 Protein by Oncoprotein MDM2.PLoS pathogens · 2016Article
- KSHV-Mediated Angiogenesis in Tumor Progression.Viruses · 2016Review
- Activation of DNA Damage Response Induced by the Kaposi's Sarcoma-Associated Herpes Virus.International journal of molecular sciences · 2016Review
- Cell Cycle Regulatory Functions of the KSHV Oncoprotein LANA.Frontiers in microbiology · 2016Review
- A Screen for Extracellular Signal-Regulated Kinase-Primed Glycogen Synthase Kinase 3 Substrates Identifies the p53 Inhibitor iASPP.Journal of virology · 2015Article
- Genomic analysis of xCT-mediated regulatory network: Identification of novel targets against AIDS-associated lymphoma.Oncotarget · 2015Article
- ORF57 overcomes the detrimental sequence bias of Kaposi's sarcoma-associated herpesvirus lytic genes.Journal of virology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kaposi's Sarcoma Herpesvirus (KSHV) is the causative agent of Kaposi's Sarcoma (KS) and two rare lymphoproliferative disorders, primary effusion lymphoma (PEL) and the plasmablastic variant of multicentric Castleman's disease (MCD). The KSHV latency-associated nuclear antigen-1 (LANA), required for the replication and maintenance of latent viral episomal DNA, is involved in the transcriptional regulation of viral and cellular genes and interacts with different cellular proteins, including the tumour suppressor p53. Here, we report that LANA also recruits the p53-related nuclear transcription factor p73, which influences cellular processes like DNA damage response, cell cycle progression and apoptosis. Both the full-length isoform TAp73α, as well as its dominant negative regulator ΔNp73α, interact with LANA. LANA affects TAp73α stability and sub-nuclear localisation, as well as TAp73α-mediated transcriptional activation of target genes. We observed that the small-molecule inhibitor Nutlin-3, which disrupts the interaction of p53 and p73 with MDM2, induces apoptotic cell death in p53 wild-type, as well as p53-mutant PEL cell lines, suggesting a possible involvement of p73. The small-molecule RETRA, which activates p73 in the context of mutant p53, leads to the induction of apoptosis in p53-mutant PEL cell lines. RNAi-mediated knockdown of p73 confirmed that these effects depend on the presence of the p73 protein. Furthermore, both Nutlin-3 and RETRA disrupt the LANA-p73 interaction in different PEL cell lines. These results suggest that LANA modulates p73 function and that the LANA-p73 interaction may represent a therapeutic target to interfere with the survival of latently KSHV-infected cells.
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