ArticleNaunyn-Schmiedeberg's archives of pharmacology2015
A therapeutic approach to treat prostate cancer by targeting Nm23-H1/h-Prune interaction.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2015. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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, 21 citations in OpenAlex.
- Long-chain fatty acyl coenzyme A inhibits NME1/2 and regulates cancer metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Aberrant expression of SPAG6 and NM23 predicts poor prognosis of human osteosarcoma.Frontiers in genetics · 2022Article
- Functional Genomics of PRUNE1 in Neurodevelopmental Disorders (NDDs) Tied to Medulloblastoma (MB) and Other Tumors.Frontiers in oncology · 2021Review
- Knockdown of neuron-specific enolase suppresses the proliferation and migration of NCI-H209 cells.Oncology letters · 2019Article
- Hepatocellular carcinoma: H-Prune gene regulatory networks.EBioMedicine · 2019Article
- Correlation of SOX9 and NM23 genes with the incidence and prognosis of prostate cancer.Oncology letters · 2019Article
- 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
- The NDPK/NME superfamily: state of the art.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- Oncogenic Epstein-Barr virus recruits Nm23-H1 to regulate chromatin modifiers.Laboratory investigation; a journal of technical methods and pathology · 2018Review
- Easy-to-use strategy for reference gene selection in quantitative real-time PCR experiments.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- Progress on Nme (NDP kinase/Nm23/Awd) gene family-related functions derived from animal model systems: studies on development, cardiovascular disease, and cancer metastasis exemplified.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Janus-faces of NME-oncoprotein interactions.Naunyn-Schmiedeberg's archives of pharmacology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nm23-H1 is a metastasis suppressor gene whose overexpression is associated with both reduced cell motility in various cancers and increased metastatic potential in neuroblastomas, osteosarcomas, and hematological malignances. We previously reported that Nm23-H1 exerts tumor suppressor action in prostate cancer cells and that h-Prune, which is overexpressed in various tumor types, binds Nm23-H1. Moreover, blockage of the Nm23-H1/h-Prune interaction with a competitive permeable peptide (CPP) attenuates migration of breast and neuroblastoma cells. This series of events suggests that the Nm23-H1/h-Prune protein complex regulates cancer progression and that its specific impairment could be a new therapeutic strategy in oncology. We found that CPP leads to inhibition of the AKT/mTORv and NF-kBv signaling pathways and also activates apoptosis. To obtain a proof-of-concept of our hypothesis, we used a xenograft model of prostate cancer to evaluate whether impairment of this complex using CPP results in an anti-tumoral effect. Using a mouse orthotopic model with bioluminescent imaging, we show evidences that CPP reduces prostate cancer metastases formation. In conclusion, CPP being able to impair formation of the h-Prune/Nm23-H1 complex holds promise for the treatment of prostate cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.