ArticleeLife2016
Nerve growth factor receptor negates the tumor suppressor p53 as a feedback regulator.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 77 citations in OpenAlex.
- A Phase II Study of the Efficacy and Safety of Oral Selinexor in Recurrent Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Trial
- An antisense-long-noncoding-RNA modulates p75iScience · 2025Article
- From neuromodulation to bone homeostasis: therapeutic targets of nerve growth factor in skeletal diseases.Frontiers in pharmacology · 2025Review
- M1 macrophages - unexpected contribution to tumor progression.Frontiers in immunology · 2025Review
- Synergistic Anti-Cancer Effects of Curcumin and Thymoquinone Against Melanoma.Antioxidants (Basel, Switzerland) · 2024Article
- Targeting BRIX1 via Engineered Exosomes Induces Nucleolar Stress to Suppress Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- A Narrative Review: Repurposing Metformin as a Potential Therapeutic Agent for Oral Cancer.Cancers · 2024Review
- Ethnicity-Based Variations in Focal Adhesion Kinase Signaling in Glioblastoma Gene Expression: A Study of the Puerto Rican Hispanic Population.International journal of molecular sciences · 2024Article
- Gene Expression Patterns Associated with Survival in Glioblastoma.International journal of molecular sciences · 2024Article
- The mechanisms of action of metformin on head and neck cancer in the pre-clinical setting: a scoping review.Frontiers in oncology · 2024Article
- Carcinogenesis and Prognostic Utility of Arginine Methylation-Related Genes in Hepatocellular Cancer.Current issues in molecular biology · 2023Article
- Ovarian stimulation with excessive FSH doses causes cumulus cell and oocyte dysfunction in small ovarian reserve heifers.Molecular human reproduction · 2023Article
- The ARTS of p53-dependent mitochondrial apoptosis.Journal of molecular cell biology · 2023Review
- Effects of multiple pro-inflammatory stimuliFrontiers in immunology · 2023Article
- MEOX2 homeobox gene promotes growth of malignant gliomas.Neuro-oncology · 2022Article
- Anticancer Effect of Cathelicidin LL-37, Protegrin PG-1, Nerve Growth Factor NGF, and Temozolomide: Impact on the Mitochondrial Metabolism, Clonogenic Potential, and Migration of Human U251 Glioma Cells.Molecules (Basel, Switzerland) · 2022Article
- Identification of Prognostic Genes in Gliomas Based on Increased Microenvironment Stiffness.Cancers · 2022Article
- Drug-Tolerant Persister Cells in Cancer Therapy Resistance.Cancer research · 2022Review
- Article
- Ubiquitin ligase DTX3 empowers mutant p53 to promote ovarian cancer development.Genes & diseases · 2022Article
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 2 institutions in 2 countries.
Funding
Abstract
Cancer develops and progresses often by inactivating p53. Here, we unveil nerve growth factor receptor (NGFR, p75NTR or CD271) as a novel p53 inactivator. p53 activates NGFR transcription, whereas NGFR inactivates p53 by promoting its MDM2-mediated ubiquitin-dependent proteolysis and by directly binding to its central DNA binding domain and preventing its DNA-binding activity. Inversely, NGFR ablation activates p53, consequently inducing apoptosis, attenuating survival, and reducing clonogenic capability of cancer cells, as well as sensitizing human cancer cells to chemotherapeutic agents that induce p53 and suppressing mouse xenograft tumor growth. NGFR is highly expressed in human glioblastomas, and its gene is often amplified in breast cancers with wild type p53. Altogether, our results demonstrate that cancers hijack NGFR as an oncogenic inhibitor of p53.
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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.