ArticleScientific reports2015
TP53 transcription factor for the NEDD9/HEF1/Cas-L gene: potential targets in Non-Small Cell Lung Cancer treatment.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- NEDD9 overexpression: Prognostic and guidance value in acute myeloid leukaemia.Journal of cellular and molecular medicine · 2021Article
- Copy Number Analysis Reveal Genetic Risks of Penile Cancer.Frontiers in oncology · 2020Article
- ZMYND10, an epigenetically regulated tumor suppressor, exerts tumor-suppressive functions via miR145-5p/NEDD9 axis in breast cancer.Clinical epigenetics · 2019Article
- Observational
- Article
- TRRUST v2: an expanded reference database of human and mouse transcriptional regulatory interactions.Nucleic acids research · 2018Article
- PRIMA-1 and PRIMA-1Cancers · 2017Review
- Effect of the p53α gene on the chemosensitivity of the H1299 human lung adenocarcinoma cell line.Oncology letters · 2017Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is a serious public health problem. Although there has been significant progress in chemotherapy, non-small cell lung cancer is still resistant to current treatments, primarily because of the slow rate of cell development. It is thus important to find new molecules directed against targets other than proliferation agents. Considering the high proportion of mutant proteins in tumor cells, and the high rate of mutation of the TP53 gene in all cancers, and in NSCLC in particular, this gene is a perfect target. Certain new molecules have been shown to restore the activity of mutated p53 protein, for example PRIMA-1, which reactivates the His273 mutant p53. In a previous study, we presented triazine A190, a molecule with a cytostatic activity that blocks cells in the G1 phase and induces apoptosis. Here, we show that A190 not only restores mutant p53 activity, but also induces an overexpression of the NEDD9 gene, leading to apoptotic death. These findings might offer hope for the development of new targeted therapies, specific to tumor cells, which spare healthy cells.
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