ArticleCells2020
IGF-1/IGF-1R/FAK/YAP Transduction Signaling Prompts Growth Effects in Triple-Negative Breast Cancer (TNBC) Cells.
Article in Cells, 2020. 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 57 papers, 3 of them syntheses 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
57 citing papers in PubMed, 3 syntheses or guidelines pooled it, 88 citations in OpenAlex.
- Pooled it
- Focal Adhesion Kinase (FAK)-Hippo/YAP transduction signaling mediates the stimulatory effects exerted by S100A8/A9-RAGE system in triple-negative breast cancer (TNBC).Journal of experimental & clinical cancer research : CR · 2022Pooled it
- Prognostic Value of Sarcopenia in Patients With Diffuse Large B-Cell Lymphoma Treated With R-CHOP: A Systematic Review and Meta-Analysis.Frontiers in nutrition · 2022Pooled it
- Blood Cell-Camouflaged Liquid Metal Nanoconjugates Orchestrate Treg Depletion and STING-Amplified Photothermal Immunity for Metastatic Triple-Negative Breast Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Overcoming IGF1R-Mediated Resistance to Oncolytic HSV1 and Radiotherapy via Triple Combination Therapy.Research square · 2025Article
- rFIP-GMI Suppresses IGF-1-Induced Invasion and Migration in Breast Cancer Cells via PI3K/Akt/β-Catenin Inhibition.Drug development research · 2025Article
- Integrative High-Throughput RNAi Screening Identifies BRSK1, STK32C and STK40 as Novel Activators of YAP/TAZ.International journal of molecular sciences · 2025Article
- IGF-1R promotes pain-like behavior in rats with myofascial pain syndrome via the PI3K/AKT pathway.Scientific reports · 2025Article
- Extracellular vesicles: the "Trojan Horse" within breast cancer host microenvironments.Molecular cancer · 2025Review
- Interleukin-1β mediates a tumor-supporting environment prompted by IGF1 in triple-negative breast cancer (TNBC).Journal of translational medicine · 2025Article
- The correlation between obesity and the occurrence and development of breast cancer.European journal of medical research · 2025Review
- Role of WAVE3 as an actin binding protein in the pathology of triple negative breast cancer.Cytoskeleton (Hoboken, N.J.) · 2025Review
- Therapeutic innovations in triple negative breast cancer: integrating molecular targeting and monoclonal antibody strategies.Frontiers in oncology · 2025Review
- Article
- P4HA1: an important target for treating fibrosis related diseases and cancer.Frontiers in pharmacology · 2024Review
- Improving efficacy of TNBC immunotherapy: based on analysis and subtyping of immune microenvironment.Frontiers in immunology · 2024Review
- Analysis of the expression and mechanism of follistatin‑like protein 1 in cervical cancer.Oncology reports · 2023Article
- Focal adhesion kinase: from biological functions to therapeutic strategies.Experimental hematology & oncology · 2023Review
- Triple Negative Breast Cancer Treatment Options and Limitations: Future Outlook.Pharmaceutics · 2023Review
- The interplay between IGF-1R signaling and Hippo-YAP in breast cancer stem cells.Cell communication and signaling : CCS · 2023Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is an aggressive breast tumor subtype that currently lacks targeted treatment options. The role played by the insulin-like growth factor-1 (IGF-1) and its cognate receptor IGF-1R in TNBC has been reported. Nevertheless, the molecular mechanisms by which the IGF-1/IGF-1R system may contribute to TNBC progression still remains to be fully understood. By computational analysis of the vast cancer genomics information in public databases (TCGA and METABRIC), we obtained evidence that high IGF-1 or IGF-1R levels correlate with a worse clinical outcome in TNBC patients. Further bioinformatics analysis revealed that both the focal adhesion and the Hippo pathways are enriched in TNBC harboring an elevated expression of IGF-1 or IGF-1R. Mechanistically, we found that in TNBC cells, the IGF-1/IGF-1R system promotes the activation of the FAK signal transduction pathway, which in turn regulates the nuclear accumulation of YAP (yes-associated protein/yes-related protein) and the expression of its target genes. At the biological level, we found that the IGF-1/IGF-1R-FAK-YAP network cascade triggers the growth potential of TNBC cells, as evaluated in different experimental systems. Overall, our results suggest that the IGF-1/IGF-1R/FAK/YAP axis may contribute to the progression of the aggressive TNBC subtype.
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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.