ArticleCarcinogenesis2008
Survivin repression by p53, Rb and E2F2 in normal human melanocytes.
Article in Carcinogenesis, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.
- Survivin promoter -31G/C (rs9904341) polymorphism and cancer susceptibility: a meta-analysis.Molecular biology reports · 2012Pooled it
- ZNF473 promotes colorectal cancer progression and chemoresistance by destabilizing p53 protein to upregulate Survivin.Cell death discovery · 2026Article
- Biomarkers of Common Molecular Dysregulation in Tumor Tissue and Peritumor Mucosa in Head and Neck SCC: Insights into Field Cancerization.International journal of molecular sciences · 2026Review
- Survivin Is a Central Mediator of Cell Proliferation in HPV-Negative Head and Neck Squamous Cell Carcinoma.Cancers · 2025Article
- Transcriptional patterns of cancer-related genes in primary and metastatic tumours revealed by machine learning.BMC biology · 2025Article
- E2F2(E2F transcription factor 2) as a potential therapeutic target in meibomian gland carcinoma: evidence from functional and epigenetic studies.BMC cancer · 2025Article
- Comparative Study of the Expressions of Nuclear (∆EX3) and Cytoplasmic (2B) Survivins in Oral Squamous Cell Carcinoma and Oral Lichen Planus Using Real-Time PCR.Clinical and experimental dental research · 2025Article
- Single-cell analysis unveils cell subtypes of acral melanoma cells at the early and late differentiation stages.Journal of Cancer · 2025Article
- Review
- Review
- The MDM2-p53 Axis Represents a Therapeutic Vulnerability Unique to Glioma Stem Cells.International journal of molecular sciences · 2024Article
- Tubulin Complexity in Cancer and Metastasis.Advances in experimental medicine and biology · 2024Review
- The role of E2F2 in cancer progression and its value as a therapeutic target.Frontiers in immunology · 2024Review
- Cell cycle regulation: p53-p21-RB signaling.Cell death and differentiation · 2022Review
- Review
- Review
- Emerging Importance of Survivin in Stem Cells and Cancer: the Development of New Cancer Therapeutics.Stem cell reviews and reports · 2020Review
- The role of survivin in the progression of pancreatic ductal adenocarcinoma (PDAC) and a novel survivin-targeted therapeutic for PDAC.PloS one · 2020Article
- Early Cellular Responses of Prostate Carcinoma Cells to Sepantronium Bromide (YM155) Involve Suppression of mTORC1 by AMPK.Scientific reports · 2019Article
- Molecular pathogenic pathways in extranodal NK/T cell lymphoma.Journal of hematology & oncology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The inhibitor of apoptosis protein survivin is a dual mediator of apoptosis resistance and cell cycle progression and is highly expressed in cancer. We have shown previously that survivin is up-regulated in melanoma compared with normal melanocytes, is required for melanoma cell viability, and that melanocyte expression of survivin predisposes mice to ultraviolet-induced melanoma and metastasis. The mechanism of survivin up-regulation in the course of melanocyte transformation and its repression in normal melanocytes, however, has not been clearly defined. We show here that p53 and retinoblastoma (Rb), at basal levels and in the absence of any activating stimuli, are both required to repress survivin transcription in normal human melanocytes. Survivin repression in melanocytes does not involve alterations in protein stability or promoter methylation. p53 and Rb (via E2Fs) regulate survivin expression by direct binding to the survivin promoter; p53 also affects survivin expression by activating p21. We demonstrate a novel role for E2F2 in the negative regulation of survivin expression. In addition, we identify a novel E2F-binding site in the survivin promoter and show that mutation of either the p53- or E2F-binding sites is sufficient to increase promoter activity. These studies suggest that compromise of either p53 or Rb pathways during melanocyte transformation leads to up-regulation of survivin expression in melanoma.
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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.