ArticleBMC cancer2015
COP1, the negative regulator of ETV1, influences prognosis in triple-negative breast cancer.
Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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
18 citing papers in PubMed, 1 synthesis or guideline pooled it.
- E3 Ubiquitin Ligases in Breast Cancer Metastasis: A Systematic Review of Pathogenic Functions and Clinical Implications.Frontiers in oncology · 2021Pooled it
- ETV1/TGF-β/SMAD4-CTGF Axis Activated Tumor-CAFs Crosstalk Promotes Poor Progression in Hepatocellular Carcinoma Patients.Cancer medicine · 2026Article
- Multiple ETS family transcription factors bind mutant p53 via distinct interaction regions.FEBS letters · 2026Article
- Ubiquitination in cancer: mechanisms and therapeutic opportunities.Cancer communications (London, England) · 2025Review
- Assessing deep learning methods in cis-regulatory motif finding based on genomic sequencing data.Briefings in bioinformatics · 2022Article
- Article
- Ubiquitin-Mediated Control of ETS Transcription Factors: Roles in Cancer and Development.International journal of molecular sciences · 2021Review
- Genomic and transcriptomic characterization of the human glioblastoma cell line AHOL1.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Article
- RFWD2 Knockdown as a Blocker to Reverse the Oncogenic Role of TRIB2 in Lung Adenocarcinoma.Frontiers in oncology · 2021Article
- Data-Driven Modeling of Breast Cancer Tumors Using Boolean Networks.Frontiers in big data · 2021Article
- The prognosis analysis ofTranslational cancer research · 2020Article
- Function and regulation of the PEA3 subfamily of ETS transcription factors in cancer.American journal of cancer research · 2020Review
- Correlation of constitutive photomorphogenic 1 (COP1) and p27 tumor suppressor protein expression in ovarian cancer.Genes & genomics · 2019Article
- High expression of PDE4D correlates with poor prognosis and clinical progression in pancreaticductal adenocarcinoma.Journal of Cancer · 2019Article
- miR-17-5p suppresses cell proliferation and invasion by targeting ETV1 in triple-negative breast cancer.BMC cancer · 2017Article
- The Ubiquitin Ligase COP1 Promotes Glioma Cell Proliferation by Preferentially Downregulating Tumor Suppressor p53.Molecular neurobiology · 2017Article
- Identification of cis-regulatory mutations generating de novo edges in personalized cancer gene regulatory networks.Genome medicine · 2017Article
- E3 ubiquitin ligase RFWD2 controls lung branching through protein-level regulation of ETV transcription factors.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundETS variant 1 (ETV1) and E3 ubiquitin ligase constitutive photomorphogenetic 1 (COP1) have been proposed to be a pair of oncogene and tumor suppressor. However, the co-existing status of ETV1 and COP1 in triple-negative breast cancer (TNBC) and their predictive role in determining the patient's outcome are uncertain.
methodsWe examined the abundance of COP1 and ETV1 proteins and their clinicopathologic significance in archival TNBC tissues from 105 patients by tissue microarray. The potential function link between COP1 and ETV1 was observed in MDA-MB-231 cells by cell proliferation, invasion and migration assays.
resultsETV1 expression was higher in TNBC tissues compared to normal tissues, while COP1 was lower. ETV1 expression was negatively associated with COP1 abundance in TNBCs. Overexpression of COP1 led to significant reduction of ETV1 in MDA-MB-231 cells, and suppressed the cells migration and invasion. Rescue of ETV1 expression in the presence of COP1 notably regained the cells behaviors. ETV1-positive group was associated with a markedly poor overall survival. Meanwhile, we had observed favourable prognosis in COP1-positive cases for the first time. Multivariate analysis showed that COP1 together with ETV1 were independent risk factors in the prognosis of TNBC patients.
conclusionsCOP1 might be a tumor suppressor by negative regulating ETV1 in patients with TNBCs. COP1 and ETV1 are a pair of independent predictors of prognosis for TNBC cases. Thus, targeting them might be a potential strategy for personalized TNBC treatment.
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.