ArticleProceedings of the National Academy of Sciences of the United States of America2000
Epidermal growth factor-induced nuclear factor kappa B activation: A major pathway of cell-cycle progression in estrogen-receptor negative breast cancer cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers, 3 of them syntheses that pooled it.
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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
120 citing papers in PubMed, 3 syntheses or guidelines pooled it, 351 citations in OpenAlex.
- Association between dietary acid load and cancer risk and prognosis: An updated systematic review and meta-analysis of observational studies.Frontiers in nutrition · 2022Pooled it
- Fruit and vegetable consumption and incident breast cancer: a systematic review and meta-analysis of prospective studies.British journal of cancer · 2021Pooled it
- Fruit and vegetable intake and risk of breast cancer by hormone receptor status.Journal of the National Cancer Institute · 2013Pooled it
- Importance of polymorphisms in NF-kappaB1 and NF-kappaBIalpha genes for melanoma risk, clinicopathological features and tumor progression in Swedish melanoma patients.Journal of cancer research and clinical oncology · 2007Trial
- Damnacanthal Suppresses Breast Cancer Cells by Inducing Apoptosis and Cell Cycle Arrest via NF-ĸB Signaling.Pharmacology research & perspectives · 2026Article
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- PPY-Induced iCAFs Cultivate an Immunosuppressive Microenvironment in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Modelling the disease: HMaterials today. Bio · 2023Article
- Article
- TFAP2C Knockdown Sensitizes Bladder Cancer Cells to Cisplatin Treatment via Regulation of EGFR and NF-κB.Cancers · 2022Article
- Revisiting Epithelial Carcinogenesis.International journal of molecular sciences · 2022Article
- Analysis of Factors Affecting 5-ALA Fluorescence Intensity in Visualizing Glial Tumor Cells-Literature Review.International journal of molecular sciences · 2022Review
- Dietary inflammatory potential, oxidative balance score, and risk of breast cancer: Findings from the Sister Study.International journal of cancer · 2021Article
- Potentiating Therapeutic Effects of Epidermal Growth Factor Receptor Inhibition in Triple-Negative Breast Cancer.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Stable Cells with NF-κB-ZsGreen Fused Genes Created by TALEN Editing and Homology Directed Repair for Screening Anti-inflammation Drugs.Journal of inflammation research · 2021Article
- Epidermal growth factor upregulates the expression of A20 in hepatic cells via the MEK1/MSK1/p-p65 (Ser276) signaling pathway.American journal of translational research · 2021Article
- Hydrogen sulfide and its donors: Novel antitumor and antimetastatic therapies for triple-negative breast cancer.Redox biology · 2020Review
- The Role of ERα36 in Development and Tumor Malignancy.International journal of molecular sciences · 2020Review
- Cancer gene therapy by NF-κB-activated cancer cell-specific expression of CRISPR/Cas9 targeting telomeres.Gene therapy · 2020Article
- Simultaneous targeting of HER family pro-survival signaling with Pan-HER antibody mixture is highly effective in TNBC: a preclinical trial with PDXs.Breast cancer research : BCR · 2020Article
60 more citing papers are in PubMed but not listed here.
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 2 institutions in 1 country.
Funding
Abstract
The epidermal growth factor (EGF) family of receptors (EGFR) is overproduced in estrogen receptor (ER) negative (-) breast cancer cells. An inverse correlation of the level of EGFR and ER is observed between ER- and ER positive (+) breast cancer cells. A comparative study with EGFR-overproducing ER- and low-level producing ER+ breast cancer cells suggests that EGF is a major growth-stimulating factor for ER- cells. An outline of the pathway for the EGF-induced enhanced proliferation of ER- human breast cancer cells is proposed. The transmission of mitogenic signal induced by EGF-EGFR interaction is mediated via activation of nuclear factor kappaB (NF-kappaB). The basal level of active NF-kappaB in ER- cells is elevated by EGF and inhibited by anti-EGFR antibody (EGFR-Ab), thus qualifying EGF as a NF-kappaB activation factor. NF-kappaB transactivates the cell-cycle regulatory protein, cyclin D1, which causes increased phosphorylation of retinoblastoma protein, more strongly in ER- cells. An inhibitor of phosphatidylinositol 3 kinase, Ly294-002, blocked this event, suggesting a role of the former in the activation of NF-kappaB by EGF. Go6976, a well-characterized NF-kappaB inhibitor, blocked EGF-induced NF-kappaB activation and up-regulation of cell-cycle regulatory proteins. This low molecular weight compound also caused apoptotic death, predominantly more in ER- cells. Thus Go6976 and similar NF-kappaB inhibitors are potentially novel low molecular weight therapeutic agents for treatment of ER- breast cancer patients.
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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.