ArticleMolecular cancer2024
Tumor-intrinsic role of ICAM-1 in driving metastatic progression of triple-negative breast cancer through direct interaction with EGFR.
Article in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Perspectives of EGFR co-targeting with nanocarriers for anti-TNBC purposes.Genes & diseases · 2026Review
- Sweetening the bonds: how O-GlcNAcylation modulates cell adhesion.Acta pharmacologica Sinica · 2026Review
- Co-Exposure to Lunasin and Other Drugs as a Potential Chemopreventive Strategy Against Breast and Colon Cancers: A Review.International journal of molecular sciences · 2026Review
- Single-nucleus sequencing dissects the malignant change of early lung adenocarcinoma: SMAD3 suppresses antitumor T cell immunity via ICAM1.NPJ precision oncology · 2026Article
- Bioinformatics Analysis of microRNAs Associated with Metastatic Potential in Breast Cancer.Biology · 2026Article
- Article
- Combinatorial inhibition of IGF2BP3-regulated receptor tyrosine kinases offers a new therapeutic strategy for triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- BMI and Breast Subcutaneous Fat: Potential Indicators for Ultrasound Diagnosis of Breast Cancer?Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine · 2026Article
- The ethyl acetate extract from Trichoderma viride fermentation acts by downregulating the leukocyte transendothelial migration signaling pathway to induce ferroptosis in triple-negative breast cancer cells.Natural products and bioprospecting · 2026Article
- Identification ofFrontiers in pharmacology · 2026Article
- Targeting the tripartite axis of immune-metabolic-spatial crosstalk to overcome therapy resistance in breast cancer.Frontiers in immunology · 2026Review
- Extracellular vesicles derived from pro-inflammatory M1 macrophages induce an inflammatory and invasive phenotype in melanoma cells.Cell communication and signaling : CCS · 2025Article
- Novel quinolinyl-thiazole hybrid candidates bearingRSC advances · 2025Article
- Integrated multi-omics identifies a CD54Molecular cancer · 2025Article
- Phytochemical Profiling, Antioxidant Activity, and In Vitro Cytotoxic Potential of MangrovePharmaceuticals (Basel, Switzerland) · 2025Article
- Integrative multi-omics analysis identifies key genes and colocalized signals associated with colorectal cancer risk.BMC cancer · 2025Article
- Subtype-specific dysregulation of biogenic amine-related genes and miRNAs in breast cancer: identification of DRD2, HRH2, and HRH4 as potential therapeutic targets in TNBC and HER2+ subtypes.Breast cancer research and treatment · 2025Article
- Long-term treatment with benzodiazepines and related Z-drugs exacerbates breast cancer: clinical evidence and molecular mechanisms.Cellular & molecular biology letters · 2025Article
- Immunotherapy biomarkers in brain metastases: insights into tumor microenvironment dynamics.Frontiers in immunology · 2025Review
- Identification of Potential Targets for EGFR-Regulated Nucleus Pulposus Degeneration Using Single-Cell RNA Sequencing and Machine Learning.Journal of inflammation research · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC), the most aggressive subtype, presents a critical challenge due to the absence of approved targeted therapies. Hence, there is an urgent need to identify effective therapeutic targets for this condition. While epidermal growth factor receptor (EGFR) is prominently expressed in TNBC and recognized as a therapeutic target, anti-EGFR therapies have yet to gain approval for breast cancer treatment due to their associated side effects and limited efficacy. Here, we discovered that intercellular adhesion molecule-1 (ICAM-1) exhibits elevated expression levels in metastatic breast cancer and serves as a pivotal binding adaptor for EGFR activation, playing a crucial role in malignant progression. The activation of EGFR by tumor-expressed ICAM-1 initiates biased signaling within the JAK1/STAT3 pathway, consequently driving epithelial-to-mesenchymal transition and facilitating heightened metastasis without influencing tumor growth. Remarkably, ICAM-1-neutralizing antibody treatment significantly suppressed cancer metastasis in a breast cancer orthotopic xenograft mouse model. In conclusion, our identification of ICAM-1 as a novel tumor intrinsic regulator of EGFR activation offers valuable insights for the development of TNBC-specific anti-EGFR therapies.
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Registered trials
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