ArticleOncogene2008
Inactivation of the Rb pathway and overexpression of both isoforms of E2F3 are obligate events in bladder tumours with 6p22 amplification.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- Genome-wide Association Study of Bladder Cancer Reveals New Biological and Translational Insights.European urology · 2023Pooled it
- Molecular biomarkers of progression in non-muscle-invasive bladder cancer - beyond conventional risk stratification.Nature reviews. Urology · 2025Review
- Possible etiological association of ovine papillomaviruses with bladder tumors in cattle.Virus research · 2023Review
- mRNA-miRNA bipartite networks reconstruction in different tissues of bladder cancer based on gene co-expression network analysis.Scientific reports · 2022Article
- Circular RNA circ_0000644 promotes papillary thyroid cancer progression via sponging miR-1205 and regulating E2F3 expression.Cell cycle (Georgetown, Tex.) · 2022Article
- Analysis of core genes for colorectal cancer prognosis based on immune and stromal scores.PeerJ · 2021Article
- The Over-Expression of E2F3 Might Serve as Prognostic Marker for Neuroblastoma Patients with Stage 4S Disease.Diagnostics (Basel, Switzerland) · 2020Article
- MiR-22 suppresses the growth and metastasis of bladder cancer cells by targeting E2F3.International journal of clinical and experimental pathology · 2020Article
- Clonal Relatedness and Mutational Differences between Upper Tract and Bladder Urothelial Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- XPO1 inhibition by selinexor induces potent cytotoxicity against high grade bladder malignancies.Oncotarget · 2018Article
- Stem-Like Signature Predicting Disease Progression in Early Stage Bladder Cancer. The Role of E2F3 and SOX4.Biomedicines · 2018Review
- Association of polymorphic markers of genesPeerJ · 2017Article
- Truncated Isoforms of lncRNA ANRIL Are Overexpressed in Bladder Cancer, But Do Not Contribute to Repression of INK4 Tumor Suppressors.Non-coding RNA · 2015Article
- MiR-377 targets E2F3 and alters the NF-kB signaling pathway through MAP3K7 in malignant melanoma.Molecular cancer · 2015Article
- Article
- Molecular biology of bladder cancer: new insights into pathogenesis and clinical diversity.Nature reviews. Cancer · 2015Review
- Sox4 Expression Confers Bladder Cancer Stem Cell Properties and Predicts for Poor Patient Outcome.International journal of biological sciences · 2015Article
- The role of microRNAs and long non-coding RNAs in the pathology, diagnosis, and management of melanoma.Archives of biochemistry and biophysics · 2014Review
- In vivo disruption of an Rb-E2F-Ezh2 signaling loop causes bladder cancer.Cancer research · 2014Article
- Retinoblastoma protein (RB) interacts with E2F3 to control terminal differentiation of Sertoli cells.Cell death & disease · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
E2F3 and CDKAL1 are candidate genes from the 6p22 region frequently amplified in bladder cancer. Expression of E2F3 isoforms (E2F3a and b) and CDKAL1 were examined and modulated in 6p22-amplified bladder cell lines. Eight lines with amplification showed overexpression of both E2F3 isoforms and CDKAL1. shRNA-mediated knockdown of CDKAL1 had no effect on proliferation. Knockdown of E2F3a or E2F3b alone induced antiproliferative effects, with the most significant effect on proliferation being observed when both isoforms were knocked down together. As E2Fs interact with the Rb tumour suppressor protein, Rb expression was analysed. There was a striking relationship between 6p22.3 amplification, E2F3 overexpression and lack of Rb expression. This was also examined in primary bladder tumours. Array-CGH detected 6p22.3 amplification in 8/91 invasive tumours. Five were studied in more detail. Four showed 13q14.2 loss (including RB1) and expressed no Rb protein. In the fifth, 13q was unaltered but the CDKN2A locus was deleted. This tumour was negative for p16 and positive for Rb protein. As p16 is a negative regulator of the Rb pathway, its loss represents an alternative mechanism for inactivation. Indeed, a phospho-specific Rb antibody showed much Rb protein in a hyperphosphorylated (inactive) form. We conclude that inactivation of the Rb pathway is required in addition to E2F3 overexpression in this subset of bladder tumours.
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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.