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JMY protein, a regulator of P53 and cytoplasmic actin filaments, is expressed in normal and neoplastic tissues
- Source :
- Virchows Archiv. 465:715-722
- Publication Year :
- 2014
- Publisher :
- Springer Science and Business Media LLC, 2014.
-
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.
- Subjects :
- Pathology
medicine.medical_specialty
Blotting, Western
Motility
Biology
Pathology and Forensic Medicine
Antibody Specificity
Neoplasms
medicine
Humans
Nuclear protein
Cytoskeleton
Molecular Biology
Actin
Oncogene
Antibodies, Monoclonal
Nuclear Proteins
Cell Biology
General Medicine
Transfection
Actin cytoskeleton
Immunohistochemistry
Cell biology
Actin Cytoskeleton
Tissue Array Analysis
Cytoplasm
MCF-7 Cells
Trans-Activators
Tumor Suppressor Protein p53
HeLa Cells
Subjects
Details
- ISSN :
- 14322307 and 09456317
- Volume :
- 465
- Database :
- OpenAIRE
- Journal :
- Virchows Archiv
- Accession number :
- edsair.doi.dedup.....135744f5a37e38845061cd5d4b6c58ff