ArticleOpen medicine (Warsaw, Poland)2024
Role of ICAM-1 in triple-negative breast cancer.
Article in Open medicine (Warsaw, Poland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- 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
- The Janus face of tissue-resident memory T cells: dual programming in tumor immune surveillance and autoimmune pathology.Frontiers in immunology · 2026Review
- Bridging pharmacovigilance and genetic insight: investigating drugs and indications for breast cancer risk in women with autoimmune diseases.Journal of translational medicine · 2025Article
- Systemic chemotherapy in metastatic TNBC polarizes effector T cell differentiation.Cancer cell international · 2025Article
- CircASH1L-mediated tumor progression in triple-negative breast cancer: PI3K/AKT pathway mechanisms.Open medicine (Warsaw, Poland) · 2025Article
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6 authors.
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Abstract
Intercellular adhesion molecule-1 (ICAM-1) is related to the occurrence and development of a variety of tumors. However, the role of ICAM-1 in the regulation of growth, metastasis, and clinical prognosis of the specific molecular subtypes of breast cancer, triple-negative breast cancer (TNBC), remains to be elucidated. This study explored the role of ICAM-1 in breast cancer and its triple-negative subtypes by systematic bioinformatics methods. The results showed that the expression of ICAM-1 in breast cancer tissues was significantly higher than that in normal tissues, especially in TNBC subtypes. In breast cancer, ICAM-1 mainly activates pathways related to apoptosis and epithelial-mesenchymal transition, while its overexpression in TNBC is associated with inflammatory response, apoptosis, and other processes. TNBC patients displaying higher ICAM-1 expression demonstrate enhanced responses to immunotherapy. High ICAM-1 expression is sensitive to drugs targeting tumor cell proliferation, apoptosis, and angiogenesis. In conclusion, breast cancer is characterized by significantly high expression of ICAM-1, with TNBC subtypes expressing ICAM-1 at much higher levels than other subtypes. The diagnosis, prognosis, development, distant metastases, and immunotherapy of TNBC are correlated with high expression of ICAM-1. This research provides available data for the further study of the diagnosis and treatment of TNBC.
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