ArticleNeoplasia (New York, N.Y.)2017
Physical and Functional Interactions between ELL2 and RB in the Suppression of Prostate Cancer Cell Proliferation, Migration, and Invasion.
Article in Neoplasia (New York, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Interactions between key genes and pathways in prostate cancer progression and therapy resistance.Frontiers in oncology · 2025Review
- Construct dysregulated miRNA-mRNA interaction networks to conjecture possible pathogenesis for Stomach adenocarcinomas.Cancer biomarkers : section A of Disease markers · 2024Article
- A compendium of Androgen Receptor Variant 7 target genes and their role in Castration Resistant Prostate Cancer.Frontiers in oncology · 2023Review
- Article
- Role of CYP3A5 in Modulating Androgen Receptor Signaling and Its Relevance to African American Men with Prostate Cancer.Cancers · 2020Article
- SIRPB1 promotes prostate cancer cell proliferation via Akt activation.The Prostate · 2020Article
- ELL2 Is Required for the Growth and Survival of AR-Negative Prostate Cancer Cells.Cancer management and research · 2020Article
- Conditional Deletion of Eaf1 Induces Murine Prostatic Intraepithelial Neoplasia in Mice.Neoplasia (New York, N.Y.) · 2019Article
- The SOX4/miR-17-92/RB1 Axis Promotes Prostate Cancer Progression.Neoplasia (New York, N.Y.) · 2019Article
- Anti-apoptotic factor Birc3 is up-regulated by ELL2 knockdown and stimulates proliferation in LNCaP cells.American journal of clinical and experimental urology · 2019Article
- Regulation of ELL2 stability and polyubiquitination by EAF2 in prostate cancer cells.The Prostate · 2018Article
- ELL2 regulates DNA non-homologous end joining (NHEJ) repair in prostate cancer cells.Cancer letters · 2018Article
- Concurrent EAF2 and ELL2 loss phenocopies individual EAF2 or ELL2 loss in prostate cancer cells and murine prostate.American journal of clinical and experimental urology · 2018Article
- Conditional deletion of ELL2 induces murine prostate intraepithelial neoplasia.The Journal of endocrinology · 2017Article
- In silico analysis suggests ELL2 as a survival-associated cross-tissue biomarker in gastric cancer.Cancer biomarkers : section A of Disease markersArticle
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Elongation factor, RNA polymerase II, 2 (ELL2) is expressed and regulated by androgens in the prostate. ELL2 and ELL-associated factor 2 (EAF2) form a stable complex, and their orthologs in Caenorhabditis elegans appear to be functionally similar. In C. elegans, the EAF2 ortholog eaf-1 was reported to interact with the retinoblastoma (RB) pathway to control development and fertility in worms. Because RB loss is frequent in prostate cancer, ELL2 interaction with RB might be important for prostate homeostasis. The present study explored physical and functional interaction of ELL2 with RB in prostate cancer. ELL2 expression in human prostate cancer specimens was detected using quantitative polymerase chain reaction coupled with laser capture microdissection. Co-immunoprecipitation coupled with deletion mutagenesis was used to determine ELL2 association with RB. Functional interaction between ELL2 and RB was tested using siRNA knockdown, BrdU incorporation, Transwell, and/or invasion assays in LNCaP, C4-2, and 22Rv1 prostate cancer cells. ELL2 expression was downregulated in high-Gleason score prostate cancer specimens. ELL2 could be bound and stabilized by RB, and this interaction was mediated through the N-terminus of ELL2 and the C-terminus of RB. Concurrent siRNA knockdown of ELL2 and RB enhanced cell proliferation, migration, and invasion as compared to knockdown of ELL2 or RB alone in prostate cancer cells. ELL2 and RB can interact physically and functionally to suppress prostate cancer progression.
Identifiers
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.