ArticleThe Journal of biological chemistry2016
AP-1 Is a Key Regulator of Proinflammatory Cytokine TNFα-mediated Triple-negative Breast Cancer Progression.
Article in The Journal of biological chemistry, 2016. 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 67 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.
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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
67 citing papers in PubMed, 134 citations in OpenAlex.
- Myeloid Activator Protein-1 Complex Contributes to Salt-Sensitive Hypertension.Circulation research · 2026Article
- The promyelocytic leukemia PML protein coordinates immune evasion in triple-negative breast cancer via independent and converging mechanisms.Cell death and differentiation · 2026Article
- Pervasive enhanced transcription in inflammatory breast cancer tumors and PBMCs impacts RNA splicing and intronic RNAs in plasma.Science advances · 2026Article
- Maternal obesity induces activator protein 1-mediated inflammatory response to impair embryonic neurogenesis.The Journal of physiology · 2026Article
- Transcription-based comparison ofMicrobiology spectrum · 2026Article
- A distinct monocyte transcriptional state links systemic immune dysregulation to pulmonary impairment in long COVID.Nature immunology · 2026Article
- Role of LIGHT in the Inflammatory Mechanisms of Psoriasis via Upregulation of Proliferation and Cytokine Production of Keratinocytes.Immunity, inflammation and disease · 2026Article
- Elevated LDL-C induces T-cell metabolic dysfunction and increases inflammation and oxidative stress in midlife adults.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- Cytokine Networks in Triple-Negative Breast Cancer: Mechanisms, Therapeutic Targets, and Emerging Strategies.Biomedicines · 2025Review
- PKC-International journal of molecular sciences · 2025Article
- Oxidative Stress: Pathological Driver in Chronic Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Chromatin accessibility and differentially expressed genes profiling in large yellow croaker (Frontiers in immunology · 2025Article
- Therapeutic innovations in triple negative breast cancer: integrating molecular targeting and monoclonal antibody strategies.Frontiers in oncology · 2025Review
- FRA1 (Frontiers in cell and developmental biology · 2025Article
- Gold and Silver Nanoparticles Efficiently Modulate the Crosstalk Between Macrophages and Cancer Cells.International journal of nanomedicine · 2025Article
- Synergistic effects of curcumin and stem cells on spinal cord injury: a comprehensive review.Molecular biology reports · 2024Review
- Matrix stiffness-dependent regulation of immunomodulatory genes in human MSCs is associated with the lncRNA CYTOR.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Multifunctional Cell Regulation Activities of the Mussel Lectin SeviL: Induction of Macrophage Polarization toward the M1 Functional Phenotype.Marine drugs · 2024Article
- An early regulatory mechanism of hyperinflammation by restricting monocyte contribution.Frontiers in immunology · 2024Article
- Relevance of Phytochemical Taste for Anti-Cancer Activity: A Statistical Inquiry.International journal of molecular sciences · 2023Review
7 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) represents a highly aggressive form of breast cancer with limited treatment options. Proinflammatory cytokines such as TNFα can facilitate tumor progression and metastasis. However, the mechanistic aspects of inflammation mediated TNBC progression remain unclear. Using ChIP-seq, we demonstrate that the cistrome for the AP-1 transcription factor c-Jun is comprised of 13,800 binding regions in TNFα-stimulated TNBC cells. In addition, we show that c-Jun regulates nearly a third of the TNFα-regulated transcriptome. Interestingly, high expression level of the c-Jun-regulated pro-invasion gene program is associated with poor clinical outcome in TNBCs. We further demonstrate that c-Jun drives TNFα-mediated increase of malignant characteristics of TNBC cells by transcriptional regulation of Ninj1. As exemplified by the CXC chemokine genes clustered on chromosome 4, we demonstrate that NF-κB might be a pioneer factor required for the regulation of TNFα-inducible inflammatory genes, whereas c-Jun has little effect. Together, our results uncover AP-1 as an important determinant for inflammation-induced cancer progression, rather than inflammatory response.
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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.