ArticleJournal of virology2009
EBNA3C can modulate the activities of the transcription factor Necdin in association with metastasis suppressor protein Nm23-H1.
Article in Journal of virology, 2009. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Nm23-H1 induces apoptosis in primary effusion lymphoma cells via inhibition of NF-κB signaling through interaction with oncogenic latent protein vFLIP K13 of Kaposi's sarcoma-associated herpes virus.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Necdin: A purposive integrator of molecular interaction networks for mammalian neuron vitality.Genes to cells : devoted to molecular & cellular mechanisms · 2021Review
- NM23-H1 Expression of Head and Neck Squamous Cell Carcinoma in Association With the Response to Irradiation.Frontiers in oncology · 2021Article
- NM23/NDPK proteins in transcription regulatory functions and chromatin modulation: emerging trends.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- The NDPK/NME superfamily: state of the art.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Clinical Implication and the Hereditary Factors of NM23 in Hepatocellular Carcinoma Based on Bioinformatics Analysis and Genome-Wide Association Study.Journal of oncology · 2018Article
- Herpes and polyoma family viruses in thyroid cancer.Oncology letters · 2016Article
- Role of EBNA-3 Family Proteins in EBV Associated B-cell Lymphomagenesis.Frontiers in microbiology · 2016Review
- Dissecting the contribution of EBNA3C domains important for EBV-induced B-cell growth and proliferation.Oncotarget · 2015Article
- Epstein-Barr virus latent antigens EBNA3C and EBNA1 modulate epithelial to mesenchymal transition of cancer cells associated with tumor metastasis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- EBNA3C regulates p53 through induction of Aurora kinase B.Oncotarget · 2015Article
- Regulation of the metastasis suppressor Nm23-H1 by tumor viruses.Naunyn-Schmiedeberg's archives of pharmacology · 2015Review
- NM23-H1 expression of head and neck squamous cell carcinoma in association with the response to cisplatin treatment.Oncotarget · 2014Article
- Impact of EBV essential nuclear protein EBNA-3C on B-cell proliferation and apoptosis.Future microbiology · 2013Review
- Article
- Review
- Protein-protein interactions: a mechanism regulating the anti-metastatic properties of Nm23-H1.Naunyn-Schmiedeberg's archives of pharmacology · 2011Review
- Epstein-Barr virus nuclear antigen 3C regulated genes in lymphoblastoid cell lines.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Tumor viruses and cancer biology: Modulating signaling pathways for therapeutic intervention.Cancer biology & therapy · 2010Review
- Nm23-H1 can induce cell cycle arrest and apoptosis in B cells.Cancer biology & therapy · 2010Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies have demonstrated the interaction between the Epstein-Barr virus (EBV) nuclear antigen 3C (EBNA3C) and the metastatic suppressor Nm23-H1 both in vitro and in vivo (C. Subramanian, M. A. Cotter II, and E. S. Robertson, Nat. Med. 7:350-355, 2001). Importantly EBNA3C can reverse the ability of Nm23-H1 to suppress migration of human cells in vitro. EBNA3C contributes to EBV-associated human cancers by regulating transcription of a number of cellular and viral promoters as well as targeting and altering the transcription activities of the metastasis suppressor Nm23-H1. Furthermore, Necdin is a cellular protein which is highly induced in terminally differentiated cells; it contributes to the regulation of cell growth and is also known to interact with viral oncoproteins. In this report, we show that Nm23-H1 and EBNA3C can modulate the biological functions of Necdin in the context of EBV infection and transformation. The levels of Necdin were consistently lower in EBV-positive cells, and EBNA3C could change the subcellular localization of Necdin as well as rescue cells from the antiangiogenic and antiproliferative effects mediated by Necdin. We also show that Necdin directly interacts with Nm23-H1, resulting in modulation of the biochemical function of Nm23-H1 as well as the biological function of Necdin. Both EBNA3C and Nm23-H1 were able to rescue not only Necdin-mediated transcriptional repression of the downstream vascular endothelial growth factor promoter but also Necdin-mediated growth suppression and antiangiogenic effects on cancer cells. The majority of this response was mediated through amino acid residues 191 to 222 of Necdin, which are also known to be important for nuclear matrix targeting. These studies suggest a role for Necdin in the regulation of downstream cellular targets in a hypoxic environment in virus-associated human cancers.
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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.