ArticleOncogene2008
Rb/E2F4 and Smad2/3 link survivin to TGF-beta-induced apoptosis and tumor progression.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 75 citations in OpenAlex.
- RNA-Seq Uncovers Association of Endocrine-Disrupting Chemicals with Hub Genes and Transcription Factors in Aggressive Prostate Cancer.International journal of molecular sciences · 2025Article
- The pivotal role of TGF-β/Smad pathway in fibrosis pathogenesis and treatment.Frontiers in oncology · 2025Review
- CDK4/6 inhibitors in breast cancer therapy: mechanisms of drug resistance and strategies for treatment.Frontiers in pharmacology · 2025Review
- Transcription factor E2F4 facilitates SUMOylation to promote HCC progression through interaction with LIN9.International journal of oncology · 2024Article
- Advances and Challenges in Targeting TGF-β Isoforms for Therapeutic Intervention of Cancer: A Mechanism-Based Perspective.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Advances in the mechanism of CDK4/6 inhibitor resistance in HR+/HER2- breast cancer.Therapeutic advances in medical oncology · 2024Review
- Progression after First-Line Cyclin-Dependent Kinase 4/6 Inhibitor Treatment: Analysis of Molecular Mechanisms and Clinical Data.International journal of molecular sciences · 2023Review
- A narrative review about CDK4/6 inhibitors in the setting of drug resistance: updates on biomarkers and therapeutic strategies in breast cancer.Translational cancer research · 2023Review
- Dioscin inhibiting EGFR-mediated Survivin expression promotes apoptosis in oral squamous cell carcinoma cells.Journal of Cancer · 2023Article
- New quinoline and isatin derivatives as apoptotic VEGFR-2 inhibitors: design, synthesis, anti-proliferative activity, docking, ADMET, toxicity, and MD simulation studies.Journal of enzyme inhibition and medicinal chemistry · 2022Article
- Design and synthesis of thiazolidine-2,4-diones hybrids with 1,2-dihydroquinolones and 2-oxindoles as potential VEGFR-2 inhibitors:Journal of enzyme inhibition and medicinal chemistry · 2022Article
- CDK4/6 inhibitor resistance mechanisms and treatment strategies (Review).International journal of molecular medicine · 2022Review
- Significance of combined TGF-β1 and survivin expression on the prognosis of patients with triple-negative breast cancer.Oncology letters · 2022Article
- Article
- Differential Expression of E2F Transcription Factors and Their Functional and Prognostic Roles in Human Prostate Cancer.Frontiers in cell and developmental biology · 2022Article
- Comprehensive analysis of the functional and prognostic value of E2F transcription factors in human prostate cancer through data mining and experimental validation.Translational cancer research · 2021Article
- Breast Cancer Resistance to Cyclin-Dependent Kinases 4/6 Inhibitors: Intricacy of the Molecular Mechanisms.Frontiers in oncology · 2021Review
- Ovarian Primary and Metastatic Tumors Suppressed by Survivin Knockout or a Novel Survivin Inhibitor.Molecular cancer therapeutics · 2019Article
- Overexpression of apoptosis-related protein, survivin, in fibroblasts from patients with systemic sclerosis.Irish journal of medical science · 2019Article
- Molecular mechanisms of resistance to CDK4/6 inhibitors in breast cancer: A review.International journal of cancer · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Survivin is a prosurvival protein overexpressed in many cancers through mechanisms that remain poorly explored, and is implicated in control of tumor progression and resistance to cancer chemotherapeutics. Here, we report a critical role for survivin in the induction of apoptosis by transforming growth factor-beta (TGF-beta). We show that TGF-beta rapidly downregulates survivin expression in prostate epithelial cells, through a unique mechanism of transcriptional suppression involving Smads 2 and 3, Rb/E2F4, and the cell-cycle repressor elements CDE and CHR. This TGF-beta response is triggered through a Smad2/3-dependent hypophosphorylation of Rb and the subsequent association of the Rb/E2F4 repressive complex to CDE/CHR elements in the proximal region of the survivin promoter. Viral-mediated gene delivery experiments, involving overexpressing or silencing survivin, reveal critical roles of survivin in apoptosis induced by TGF-beta alone or in cooperation with cancer therapeutic agents. We propose a novel TGF-beta/Rb/survivin axis with a putative role in the functional switch of TGF-beta from tumor suppressor to tumor promoter.
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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.