ReviewFEBS letters2011
Functional modulation of the metastatic suppressor Nm23-H1 by oncogenic viruses.
Review in FEBS letters, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- The interplay between Epstein-Bar virus (EBV) with the p53 and its homologs during EBV associated malignancies.Heliyon · 2019Review
- Foot-and-mouth disease virus induces lysosomal degradation of NME1 to impair p53-regulated interferon-inducible antiviral genes expression.Cell death & disease · 2018Article
- Oncogenic Epstein-Barr virus recruits Nm23-H1 to regulate chromatin modifiers.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Nm23-H1 was involved in regulation of KAI1 expression in high-metastatic lung cancer cells L9981.Journal of thoracic disease · 2016Article
- The Role of Gammaherpesviruses in Cancer Pathogenesis.Pathogens (Basel, Switzerland) · 2016Review
- 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
- Janus-faces of NME-oncoprotein interactions.Naunyn-Schmiedeberg's archives of pharmacology · 2015Review
- Epstein-Barr virus latent genes.Experimental & molecular medicine · 2015Review
- c-Abl and Arg induce cathepsin-mediated lysosomal degradation of the NM23-H1 metastasis suppressor in invasive cancer.Oncogene · 2014Article
- Impact of EBV essential nuclear protein EBNA-3C on B-cell proliferation and apoptosis.Future microbiology · 2013Review
- Nucleoside-diphosphate-kinase: a pleiotropic effector in microbial colonization under interdisciplinary characterization.Microbes and infection · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Evidence over the last two decades from a number of disciplines has solidified some fundamental concepts in metastasis, a major contributor to cancer associated deaths. However, significant advances have been made in controlling this critical cellular process by focusing on targeted therapy. A key set of factors associated with this invasive phenotype is the nm23 family of over twenty metastasis-associated genes. Among the eight known isoforms, Nm23-H1 is the most studied potential anti-metastatic factor associated with human cancers. Importantly, a growing body of work has clearly suggested a critical role for Nm23-H1 in limiting tumor cell motility and progression induced by several tumor viruses, including Epstein-Barr virus (EBV), Kaposi's sarcoma associated herpes virus (KSHV) and human papilloma virus (HPV). A more in depth understanding of the interactions between tumor viruses encoded antigens and Nm23-H1 will facilitate the elucidation of underlying mechanism(s) which contribute to virus-associated cancers. Here, we review recent studies to explore the molecular links between human oncogenic viruses and progression of metastasis, in particular the deregulation of Nm23-H1 mediated suppression.
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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.