ArticleVirchows Archiv : an international journal of pathology2014
JMY protein, a regulator of P53 and cytoplasmic actin filaments, is expressed in normal and neoplastic tissues.
Article in Virchows Archiv : an international journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Changes of Ex Vivo Cervical Epithelial Cells Due to Electroporation with JMY.International journal of molecular sciences · 2023Article
- The p53 and Calcium Regulated Actin Rearrangement in Model Cells.International journal of molecular sciences · 2022Article
- The actin nucleation factors JMY and WHAMM enable a rapid Arp2/3 complex-mediated intrinsic pathway of apoptosis.PLoS genetics · 2021Article
- Gene expression signature predicts relapse in adult patients with cytogenetically normal acute myeloid leukemia.Blood advances · 2021Article
- Role of Junction-Mediating and Regulatory Protein in the Pathogenesis of Glucocorticoid-Induced Endothelial Cell Lesions.Orthopaedic surgery · 2020Article
- High expression ofWorld journal of gastroenterology · 2019Article
- The Role of JMY in p53 Regulation.Cancers · 2018Review
- Actin Cross-Linking Toxin Is a Universal Inhibitor of Tandem-Organized and Oligomeric G-Actin Binding Proteins.Current biology : CB · 2018Article
- Actin nucleation by WH2 domains at the autophagosome.Nature communications · 2015Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
JMY is a p300-binding protein with dual action: by enhancing P53 transcription in the nucleus, it plays an important role in the cellular response to DNA damage, while by promoting actin filament assembly in the cytoplasm; it induces cell motility in vitro. Therefore, it has been argued that, depending of the cellular setting, it might act either as tumor suppressor or as oncogene. In order to further determine its relevance to human cancer, we produced the monoclonal antibody HMY 117 against a synthetic peptide from the N-terminus region and characterized it on two JMY positive cell lines, MCF7 and HeLa, wild type and after transfection with siRNA to switch off JMY expression. JMY was expressed in normal tissues and heterogeneously in different tumor types, with close correlation between cytoplasmic and nuclear expression. Most noticeable was the loss of expression in some infiltrating carcinomas compared to normal tissue and in in situ carcinomas of the breast, which is consistent with a putative suppressor role. However, as in lymph node metastases, expression of JMY was higher than in primary colorectal and head and neck carcinomas, it might also have oncogenic properties depending on the cellular context by increasing motility and metastatic potential.
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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.