ArticleNature communications2019
Death effector domain-containing protein induces vulnerability to cell cycle inhibition in triple-negative breast cancer.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Unraveling Biomarker Signatures in Triple-Negative Breast Cancer: A Systematic Review for Targeted Approaches.International journal of molecular sciences · 2024Pooled it
- Precision Nutrition as the Concept of Dietary and Nutritional Interventions for Patients With Malignancies: A Narrative Literature Review and Perspectives.Cancer reports (Hoboken, N.J.) · 2026Review
- High Throughput Characterization of Eukaryotic 2A-Like Peptides Identifies Novel Leucine-Associated Reduction in Protein Abundance.bioRxiv : the preprint server for biology · 2026Article
- Article
- Targeting G9a Exerts Pleiotropic Suppression in Triple-Negative Breast Cancer Cells: Cooperatively Inducing Pyroptosis and Apoptosis.Biomolecules · 2026Article
- Integrating axis quantitative trait loci looks beyond cell types and offers insights into brain-related traits.Nature communications · 2025Article
- Cell Settling, Migration, and Stochastic Cancer Gene Expression Suggest Potassium Membrane Flux May Initiate pH Reversal.Biomolecules · 2025Article
- Nanomaterial-assisted CRISPR gene-engineering - A hallmark for triple-negative breast cancer therapeutics advancement.Materials today. Bio · 2022Review
- Developing dietary interventions as therapy for cancer.Nature reviews. Cancer · 2022Review
- Small nucleolar RNA host gene 3 functions as a novel biomarker in liver cancer and other tumour progression.World journal of gastroenterology · 2022Review
- Triple-negative breast cancer: new treatment strategies in the era of precision medicine.Science China. Life sciences · 2021Review
- Potential Prospect of CDK4/6 Inhibitors in Triple-Negative Breast Cancer.Cancer management and research · 2021Review
- Sustained mTORC1 activity during palbociclib-induced growth arrest triggers senescence in ER+ breast cancer cells.Cell cycle (Georgetown, Tex.) · 2021Article
- Alantolactone suppresses human osteosarcoma through the PI3K/AKT signaling pathway.Molecular medicine reports · 2020Article
- Systematic mapping of cancer cell target dependencies using high-throughput drug screening in triple-negative breast cancer.Computational and structural biotechnology journal · 2020Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
Lacking targetable molecular drivers, triple-negative breast cancer (TNBC) is the most clinically challenging subtype of breast cancer. In this study, we reveal that Death Effector Domain-containing DNA-binding protein (DEDD), which is overexpressed in > 60% of TNBCs, drives a mitogen-independent G1/S cell cycle transition through cytoplasm localization. The gain of cytosolic DEDD enhances cyclin D1 expression by interacting with heat shock 71 kDa protein 8 (HSC70). Concurrently, DEDD interacts with Rb family proteins and promotes their proteasome-mediated degradation. DEDD overexpression renders TNBCs vulnerable to cell cycle inhibition. Patients with TNBC have been excluded from CDK 4/6 inhibitor clinical trials due to the perceived high frequency of Rb-loss in TNBCs. Interestingly, our study demonstrated that, irrespective of Rb status, TNBCs with DEDD overexpression exhibit a DEDD-dependent vulnerability to combinatorial treatment with CDK4/6 inhibitor and EGFR inhibitor in vitro and in vivo. Thus, our study provided a rationale for the clinical application of CDK4/6 inhibitor combinatorial regimens for patients with TNBC.
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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.