ArticleJournal of cellular and molecular medicine2009
E2F1 represses beta-catenin/TCF activity by direct up-regulation of Siah1.
Article in Journal of cellular and molecular medicine, 2009. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
- The Role of WDR77 in Cancer: More than a PRMT5 Interactor.Molecular cancer research : MCR · 2025Review
- Reactive oxygen species-induced SIAH1 promotes granulosa cells' senescence in premature ovarian failure.Journal of cellular and molecular medicine · 2022Article
- Review
- Mutant p53 Gain-of-Function: Role in Cancer Development, Progression, and Therapeutic Approaches.Frontiers in cell and developmental biology · 2020Review
- PHF19 promotes the proliferation, migration, and chemosensitivity of glioblastoma to doxorubicin through modulation of the SIAH1/β-catenin axis.Cell death & disease · 2018Article
- Plakoglobin restores tumor suppressor activity of p53Cancer science · 2018Article
- Up-regulation of Siah1 by ethanol triggers apoptosis in neural crest cells through p38 MAPK-mediated activation of p53 signaling pathway.Archives of toxicology · 2017Article
- Article
- Diminution of signal transducer and activator of transcription 3 signaling inhibits vascular permeability and anaphylaxis.The Journal of allergy and clinical immunology · 2016Article
- Regulators and effectors of Siah ubiquitin ligases.Cell biochemistry and biophysics · 2013Review
- SIAH proteins: critical roles in leukemogenesis.Leukemia · 2013Review
- Gene regulatory network inference: evaluation and application to ovarian cancer allows the prioritization of drug targets.Genome medicine · 2012Article
- Recognition of unmodified histone H3 by the first PHD finger of bromodomain-PHD finger protein 2 provides insights into the regulation of histone acetyltransferases monocytic leukemic zinc-finger protein (MOZ) and MOZ-related factor (MORF).The Journal of biological chemistry · 2011Article
- MicroRNA-149*, a p53-responsive microRNA, functions as an oncogenic regulator in human melanoma.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- E2F1 suppresses Wnt/β-catenin activity through transactivation of β-catenin interacting protein ICAT.Oncogene · 2011Article
- MicroRNA roles in beta-catenin pathway.Molecular cancer · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription factor E2F1 is a key regulator of cell proliferation and apoptosis. Its activity is strictly controlled by the pRB/E2F pathway. In the majority of cancer cells, however, this pathway is frequently found deregulated, and the underlying mechanism involving transcriptional control by E2F1 has not yet been fully elucidated. Here we report the identification of two putative E2F1-binding sites located upstream from Siah1 transcription start site (+1). Chromatin immunoprecipitation assay reveals that transcription factor E2F1 is capable of binding to the putative sites, and luciferase reporter assay shows that E2F1 can activate transcription from the Siah1 promoter. Ectopic expression of E2F1 elevates the Siah1 level, hence suppressing the beta-catenin/TCF activity. Consistently, knock-down of endogenous E2F1 by a shRNA strategy results in reduced expression of Siah1. Moreover, repression of beta-catenin/TCF activity by E2F1 can be attenuated by shRNA-based repression of endogenous Siah1, implying that Siah1 is a bona fide E2F1 target gene, which at least partly, mediates the suppression of beta-catenin/TCF signalling pathway.
Indexed as
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.