ReviewGenes2023
Deregulated E2F Activity as a Cancer-Cell Specific Therapeutic Tool.
Review in Genes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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
16 citing papers in PubMed, 22 citations in OpenAlex.
- Ru3: a novel ruthenium-based compound overcomes cisplatin resistance in non-small cell lung cancer via the E2F2-IGFBP3-GPX4 pathway.Apoptosis : an international journal on programmed cell death · 2026Article
- Genome-Wide DNA Methylation Profiling Reveals Ancestry-Associated Epigenetic Reprogramming in Cervical Intraepithelial Neoplasia.International journal of molecular sciences · 2026Article
- Cancer in transition: discovery of tumor-intrinsic transcriptional programs shaping the immune and microenvironmental landscape.Biomarker research · 2026Review
- Distinct Regulation of theCells · 2026Article
- Exploring the Dynamic Changes of Intercellular Connections in Cervical Cancer: Insights From Transcriptomic Data Combined With Single-Cell Sequencing.Human mutation · 2026Article
- hsa-let-7b-5p-associated BUB1/TMPO-AS1 ceRNA axis identified as a potential biomarker in lung adenocarcinoma.Cell division · 2025Article
- Article
- Regulation of PD-L1 Expression by SAHA-Mediated Histone Deacetylase Inhibition in Lung Cancer Cells.Cancers · 2025Article
- The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025Review
- Integrative multi-omics analysis and experimental validation identify molecular subtypes, prognostic signature, and CA9 as a therapeutic target in oral squamous cell carcinoma.Frontiers in cell and developmental biology · 2025Article
- Adenoviral Therapy for Cervical Cancer: From Targeted Modification to Immunotherapy.Anti-cancer agents in medicinal chemistry · 2025Review
- DEK regulates B-cell proliferative capacity and is associated with aggressive disease in low-grade B-cell lymphomas.Blood cancer journal · 2024Article
- Multiomics analysis identifies oxidative phosphorylation as a cancer vulnerability arising from myristoylation inhibition.Journal of translational medicine · 2024Article
- Gains of 20q11.21 in human pluripotent stem cells: Insights from cancer research.Stem cell reports · 2024Review
- PPP1R14B as a potential biomarker for the identification of diagnosis and prognosis affecting tumor immunity, proliferation and migration in prostate cancer.Journal of Cancer · 2024Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor E2F, the principal target of the tumor suppressor pRB, plays crucial roles in cell proliferation and tumor suppression. In almost all cancers, pRB function is disabled, and E2F activity is enhanced. To specifically target cancer cells, trials have been undertaken to suppress enhanced E2F activity to restrain cell proliferation or selectively kill cancer cells, utilizing enhanced E2F activity. However, these approaches may also impact normal growing cells, since growth stimulation also inactivates pRB and enhances E2F activity. E2F activated upon the loss of pRB control (deregulated E2F) activates tumor suppressor genes, which are not activated by E2F induced by growth stimulation, inducing cellular senescence or apoptosis to protect cells from tumorigenesis. Deregulated E2F activity is tolerated in cancer cells due to inactivation of the ARF-p53 pathway, thus representing a feature unique to cancer cells. Deregulated E2F activity, which activates tumor suppressor genes, is distinct from enhanced E2F activity, which activates growth-related genes, in that deregulated E2F activity does not depend on the heterodimeric partner DP. Indeed, the ARF promoter, which is specifically activated by deregulated E2F, showed higher cancer-cell specific activity, compared to the E2F1 promoter, which is also activated by E2F induced by growth stimulation. Thus, deregulated E2F activity is an attractive potential therapeutic tool to specifically target cancer cells.
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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.