ArticleNature communications2021
ICAM1 initiates CTC cluster formation and trans-endothelial migration in lung metastasis of breast cancer.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 1 of them a synthesis that pooled it.
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Who cites it
150 citing papers in PubMed, 1 synthesis or guideline pooled it, 252 citations in OpenAlex.
- The translational chasm in machine learning for triple-negative breast cancer: a quantitative landscape assessment.Frontiers in oncology · 2026Pooled it
- An endoplasmic reticulum-enriched nanogel couples ferroptotic tumor damage with macrophage reprogramming for triple-negative breast cancer immunotherapy.Bioactive materials · 2027Article
- Preclinical evaluation of trastuzumab deruxtecan in a new HER2+ leptomeningeal colonization model.Cancer letters · 2026Article
- Micro/Nanostructured Materials and Microfluidic Diagnostic Platforms Enable Multimodal Detection of Circulating Tumor Cells.Exploration (Beijing, China) · 2026Review
- Towards liquid biopsy-based analysis of antitumour immunity.Nature reviews. Clinical oncology · 2026Review
- Article
- Loss of endothelial cell FAK represses cisplatin-induced vascular senescence in distal niches to reduce lung metastatic burden.Research square · 2026Article
- Umbelliprenin co-formulated with selenium nanoparticles downregulates MMP-2, MMP-9 and ICAM-1 expression in triple-negative breast cancer cells MDA-MB-231.BMC complementary medicine and therapies · 2026Article
- Programmed cell death and metastatic evolution in breast cancer: the role of anoikis, necroptosis, and ferroptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- The vascular niche: an orchestrator of the spatiotemporal dynamics of distant metastasis.Acta pharmacologica Sinica · 2026Review
- Platelet-neutrophil cooperation in cancer: mechanisms of metastatic niche formation and implications for prognostic stratification and therapy.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Toxic lipid-induced epigenetic activation of ICAM1 in liver sinusoidal endothelium regulates myeloid-driven fibro-inflammatory response in MASH.Hepatology (Baltimore, Md.) · 2026Article
- Bioinformatics Analysis of microRNAs Associated with Metastatic Potential in Breast Cancer.Biology · 2026Article
- Suppression of Tumor Aggression Through Metabolic Reprogramming via Oxamate Targeting LDHA.International journal of molecular sciences · 2026Review
- Chromatin unwinding state for in situ identification and lineage tracing of circulating tumor cells.iMeta · 2026Article
- Is cancer the result of uncontrolled cellular growth? a glance into the tumorigenic process.Cancer cell international · 2026Review
- Article
- Preclinical models of breast cancer metastasis: strengths, limitations, and clinical relevance.NPJ breast cancer · 2026Review
- Circulating Tumor Cells: Emerging Frontiers in Cancer Technology.Expert reviews in molecular medicine · 2026Review
- From Cerebrovascular Injury to Brain Cancer: The Role of Blood-Brain Barrier Dysfunction.Biomedicines · 2026Review
90 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
22 authors at 3 institutions in 1 country.
Funding
Abstract
Circulating tumor cell (CTC) clusters mediate metastasis at a higher efficiency and are associated with lower overall survival in breast cancer compared to single cells. Combining single-cell RNA sequencing and protein analyses, here we report the profiles of primary tumor cells and lung metastases of triple-negative breast cancer (TNBC). ICAM1 expression increases by 200-fold in the lung metastases of three TNBC patient-derived xenografts (PDXs). Depletion of ICAM1 abrogates lung colonization of TNBC cells by inhibiting homotypic tumor cell-tumor cell cluster formation. Machine learning-based algorithms and mutagenesis analyses identify ICAM1 regions responsible for homophilic ICAM1-ICAM1 interactions, thereby directing homotypic tumor cell clustering, as well as heterotypic tumor-endothelial adhesion for trans-endothelial migration. Moreover, ICAM1 promotes metastasis by activating cellular pathways related to cell cycle and stemness. Finally, blocking ICAM1 interactions significantly inhibits CTC cluster formation, tumor cell transendothelial migration, and lung metastasis. Therefore, ICAM1 can serve as a novel therapeutic target for metastasis initiation of TNBC.
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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.