ArticleEBioMedicine2017
CPSF6 is a Clinically Relevant Breast Cancer Vulnerability Target: Role of CPSF6 in Breast Cancer.
Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Unraveling Biomarker Signatures in Triple-Negative Breast Cancer: A Systematic Review for Targeted Approaches.International journal of molecular sciences · 2024Pooled it
- Article
- ADAR1-mediated RNA editing in breast cancer: molecular mechanisms and therapeutic implications.Medical oncology (Northwood, London, England) · 2025Review
- Fateful Decisions of Where to Cut the Line: Pathology Associated with Aberrant 3' End Processing and Transcription Termination.Journal of molecular biology · 2025Review
- Impact of prolactin treatment on enhancing the cellular responses of MCF7 breast cancer cells to tamoxifen treatment.Discover oncology · 2024Article
- Discovery of Novel Biomarkers with Extended Non-Coding RNA Interactor Networks from Genetic and Protein Biomarkers.International journal of molecular sciences · 2024Article
- HIV-1-induced translocation of CPSF6 to biomolecular condensates.Trends in microbiology · 2024Review
- Downregulation of CPSF6 leads to global mRNA 3' UTR shortening and enhanced antiviral immune responses.PLoS pathogens · 2024Article
- The role of dsRNA A-to-I editing catalyzed by ADAR family enzymes in the pathogeneses.RNA biology · 2024Review
- Negative Regulation of CPSF6 Suppresses the Warburg Effect and Angiogenesis Leading to Tumor Progression Via c-Myc Signaling Network: Potential Therapeutic Target for Liver Cancer Therapy.International journal of biological sciences · 2024Article
- The role of alternative polyadenylation in breast cancer.Frontiers in genetics · 2024Review
- RNA-binding protein CPSF6 regulates IBSP to affect pyroptosis in gastric cancer.World journal of gastrointestinal oncology · 2023Article
- The roles of CPSF6 in proliferation, apoptosis and tumorigenicity of lung adenocarcinoma.Aging · 2022Article
- RNA Editing Enzyme ADAR1 Regulates METTL3 in an Editing Dependent Manner to Promote Breast Cancer Progression via METTL3/ARHGAP5/YTHDF1 Axis.International journal of molecular sciences · 2022Article
- ALYREF, a novel factor involved in breast carcinogenesis, acts through transcriptional and post-transcriptional mechanisms selectively regulating the short NEAT1 isoform.Cellular and molecular life sciences : CMLS · 2022Article
- Deregulated expression and subcellular localization of CPSF6, a circRNA-binding protein, promote malignant development of esophageal squamous cell carcinoma.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2022Article
- MYC Inhibition Halts Metastatic Breast Cancer Progression by Blocking Growth, Invasion, and Seeding.Cancer research communications · 2022Article
- Mutational signatures representative transcriptomic perturbations in hepatocellular carcinoma.Frontiers in genetics · 2022Article
- Atypical Rearrangements in APL-Like Acute Myeloid Leukemias: Molecular Characterization and Prognosis.Frontiers in oncology · 2022Review
- Terminal differentiation and anti-tumorigenic effects of prolactin in breast cancer.Frontiers in endocrinology · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer represents a major health challenge. The majority of breast cancer deaths are due to cancer progression/recurrence for which no efficient therapies exist. Aggressive breast cancers are characterized by loss of cellular differentiation. Defining molecular mechanisms/targets contributing to cancer aggressiveness is needed to guide the design of new screening and targeted treatments. Here, we describe a novel tumor promoting function for the Cleavage and Polyadenylation Factor-6 (CPSF6). Importantly, aggressive breast cancer cells of luminal B, HER2-overexpressing and triple negative subtypes show dependency on CPSF6 for viability and tumorigenic capacity. Mechanistically, we found CPSF6 to interact with components of the A-to-I RNA editing machinery, paraspeckles and ADAR1 enzyme, and to be required for their physical integrity. Clinically, we found CPSF6 and all core paraspeckles proteins to be overexpressed in human breast cancer cases and their expression to correlate with poor patient outcomes. Finally, we found prolactin, a key mammary differentiation factor, to suppress CPSF6/RNA editing activity. Together, this study revealed CPSF6 as a molecular target with clinical relevance for prognosis and therapy in breast cancer.
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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.