ArticleCell communication and signaling : CCS2024
Mechanisms underlying neutrophils adhesion to triple-negative breast cancer cells via CD11b-ICAM1 in promoting breast cancer progression.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
12 citing papers in PubMed.
- Irgm1 Improves Postinfarction Cardiac Repair by Promoting Neutrophil Clearance and Efferocytosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Integrated multi-omics identifies a CD54Molecular cancer · 2025Article
- N1 and N2 neutrophil subtypes in breast cancer: functional implications and clinical perspectives: a narrative review.Annals of medicine and surgery (2012) · 2025Review
- The balance between N1 and N2 neutrophils implications for breast cancer immunotherapy: a narrative review.Annals of medicine and surgery (2012) · 2025Review
- Neutrophils as key regulators of tumor microenvironment in breast cancer: a focus on N1 and N2 polarization.Annals of medicine and surgery (2012) · 2025Review
- A Novel Ferroptosis-Related Gene Prognosis Signature and Identifying Atorvastatin as a Potential Therapeutic Agent for Hepatocellular Carcinoma.Current issues in molecular biology · 2025Article
- Harnessing myeloid cells in cancer.Molecular cancer · 2025Review
- Early capecitabine metronomic chemotherapy improves patient prognosis and safety in early-stage triple-negative breast cancer.American journal of translational research · 2025Article
- N2 Neutrophils and Tumor Progression in Breast Cancer: Molecular Pathways and Implications.Breast cancer (Dove Medical Press) · 2025Review
- Construction of a prognostic survival model with tumor immune-related genes for breast cancer.Translational cancer research · 2024Article
- Prognostic Significance of CD11b-, CD8-, and CD163-Positive Tumor-Infiltrating Immune Cells in Distal Bile Duct Cancer.Journal of personalized medicine · 2024Article
- A Neutrophil-Based Predictive Model for Axillary De-Escalation After Neoadjuvant Therapy in Node-Positive Breast Cancer.IET systems biologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundTriple-negative breast cancer (TNBC) is recognized as the most aggressive and immunologically infiltrated subtype of breast cancer. A high circulating neutrophil-to-lymphocyte ratio (NLR) is strongly linked to a poor prognosis among patients with breast cancer, emphasizing the critical role of neutrophils. Although the involvement of neutrophils in tumor metastasis is well documented, their interactions with primary tumors and tumor cells are not yet fully understood.
methodsClinical data were analyzed to investigate the role of neutrophils in breast cancer. In vivo mouse model and in vitro co-culture system were used for mechanism researches. Blocking experiments were further performed to identify therapeutic agents against TNBC.
resultsTNBC cells secreted GM-CSF to sustain the survival of mature neutrophils and upregulated CD11b expression. Through CD11b, neutrophils specifically binded to ICAM1 on TNBC cells, facilitating adhesion. Transcriptomic sequencing combined with human and murine functional experiments revealed that neutrophils, through direct CD11b-ICAM1 interactions, activated the MAPK signaling pathway in TNBC cells, thereby enhancing tumor cell invasion and migration. Atorvastatin effectively inhibited ICAM1 expression in tumor cells, and tumor cells with ICAM1 knockout or treated with atorvastatin were unresponsive to neutrophil activation. The MAPK pathway and MMP9 expression were significantly inhibited in the tumor tissues of TNBC patients treated with atorvastatin.
conclusionsTargeting CD11b-ICAM1 with atorvastatin represented a potential clinical approach to reduce the malignant characteristics of TNBC.
Indexed as
Identifiers
What OpenQuestion holds
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.