ArticleOncogene2001
Amplification and overexpression of PRUNE in human sarcomas and breast carcinomas-a possible mechanism for altering the nm23-H1 activity.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 56 citations in OpenAlex.
- Targeting Group 3 Medulloblastoma by the Anti-PRUNE-1 and Anti-LSD1/KDM1A Epigenetic Molecules.International journal of molecular sciences · 2024Article
- Prune-1 drives polarization of tumor-associated macrophages (TAMs) within the lung metastatic niche in triple-negative breast cancer.iScience · 2021Article
- A competitive cell-permeable peptide impairs Nme-1 (NDPK-A) and Prune-1 interaction: therapeutic applications in cancer.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Oncogenic Epstein-Barr virus recruits Nm23-H1 to regulate chromatin modifiers.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Neuroblastoma tumorigenesis is regulated through the Nm23-H1/h-Prune C-terminal interaction.Scientific reports · 2013Article
- Essential gene profiles in breast, pancreatic, and ovarian cancer cells.Cancer discovery · 2012Article
- Review
- Protein-protein interactions: a mechanism regulating the anti-metastatic properties of Nm23-H1.Naunyn-Schmiedeberg's archives of pharmacology · 2011Review
- Molecular alterations in key-regulator genes among patients with T4 breast carcinoma.BMC cancer · 2010Article
- Regulators affecting the metastasis suppressor activity of Nm23-H1.Molecular and cellular biochemistry · 2009Review
- The Nm23-H1-h-Prune complex in cellular physiology: a 'tip of the iceberg' protein network perspective.Molecular and cellular biochemistry · 2009Review
- Genetic aberrations in soft tissue leiomyosarcoma.Cancer letters · 2009Review
- Clinical-translational approaches to the Nm23-H1 metastasis suppressor.Clinical cancer research : an official journal of the American Association for Cancer Research · 2008Review
- Phosphorylation of nm23-H1 by CKI induces its complex formation with h-prune and promotes cell motility.Oncogene · 2008Article
- Domain mapping on the human metastasis regulator protein h-Prune reveals a C-terminal dimerization domain.The Biochemical journal · 2007Article
- Increased expression of h-prune is associated with tumor progression and poor survival in gastric cancer.Cancer science · 2007Article
- Genomic analyses of transcription factor binding, histone acetylation, and gene expression reveal mechanistically distinct classes of estrogen-regulated promoters.Molecular and cellular biology · 2007Article
- Protein phosphorylation corrects the folding defect of the neuroblastoma (S120G) mutant of human nucleoside diphosphate kinase A/Nm23-H1.The Biochemical journal · 2007Article
- Expression analysis of imbalanced genes in prostate carcinoma using tissue microarrays.British journal of cancer · 2007Article
- Understanding h-prune biology in the fight against cancer.Clinical & experimental metastasis · 2007Review
Corrections and comments
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Authors and funding
21 authors at 4 institutions in 5 countries.
Funding
Abstract
PRUNE, the human homologue of the Drosophila gene, is located in 1q21.3, a region highly amplified in human sarcomas, malignant tumours of mesenchymal origin. Prune protein interacts with the metastasis suppressor nm23-H1, but shows impaired affinity towards the nm23-H1 S120G mutant associated with advanced neuroblastoma. Based on these observations, we previously suggested that prune may act as a negative regulator of nm23-H1 activity. We found amplification of PRUNE in aggressive sarcoma subtypes, such as leiomyosarcomas and malignant fibrous histiocytomas (MFH) as well as in the less malignant liposarcomas. PRUNE amplification was generally accompanied by high mRNA and moderate to high protein levels. The sarcoma samples expressed nm23-H1 mostly at low or moderate levels, whereas mRNA and protein levels were moderate to high in breast carcinomas. For the more aggressive sarcoma subtypes, 9/13 patients with PRUNE amplification developed metastases. A similar situation was observed in all breast carcinomas with amplification of PRUNE. Infection of NIH3T3 cells with a PRUNE recombinant retrovirus increased cell proliferation. Possibly, amplification and overexpression of PRUNE has the same effect in the tumours. We suggest that amplification and overexpression of PRUNE could be a mechanism for inhibition of nm23-H1 activity that affect the development or progression of these tumours.
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