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C-FOS promotes the formation of neutrophil extracellular traps and the recruitment of neutrophils in lung metastasis of triple-negative breast cancer
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C-FOS promotes the formation of neutrophil extracellular traps and the recruitment of neutrophils in lung metastasis of triple-negative breast cancer
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C-FOS promotes the formation of neutrophil extracellular traps and the recruitment of neutrophils in lung metastasis of triple-negative breast cancer
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Journal Article
C-FOS promotes the formation of neutrophil extracellular traps and the recruitment of neutrophils in lung metastasis of triple-negative breast cancer
2025
Overview
Background
Neutrophil extracellular traps (NETs) are composed of DNA chains from neutrophils and associated proteolytic enzymes, which play an important role in cancer metastasis. However, the molecular mechanism of NET-mediated lung metastasis in triple-negative breast cancer (TNBC) remains unclear.
Methods
The expression levels of NETs in breast cancer specimens and serum were analyzed and compared with normal samples. Single-cell sequencing bioinformatics analysis was conducted to identify differentially expressed genes and functional enrichment related to NET formation in patients with breast cancer. The effects of c-FOS on neutrophil recruitment and NET formation in TNBC were investigated. The upstream and downstream regulatory mechanisms mediated by c-FOS were explored through in vitro and in vivo experiments. Therapeutic approaches targeting c-FOS for treating TNBC were further studied.
Results
Inhibition of c-FOS can suppress tumor growth and lung metastasis in TNBC. Mechanistically, c-FOS promotes transcription by binding to the PAD4 promoter region, facilitating the formation of NETs. Additionally, the activation of the ROS-p38 pathway further enhances c-FOS expression. High expression of c-FOS also promotes the expression of inflammatory factors, facilitating neutrophil recruitment. Both in vitro and in vivo experiments demonstrated that the application of T5224 effectively inhibits the formation of NETs, suppressing lung metastasis and tumor growth.
Conclusion
In summary, this study demonstrates that the ROS-p38-cFOS-PAD4 axis can increase NET formation in TNBC and promote the expression of inflammatory factors, facilitating neutrophil recruitment. Therefore, targeting this pathway may help inform new therapeutic strategies and provide new insights for immunotherapy in TNBC.
Publisher
BioMed Central,BioMed Central Ltd,Springer Nature B.V,BMC
Subject
/ Biomedical and Life Sciences
/ c-FOS
/ Cancer
/ Cells
/ Extracellular Traps - metabolism
/ Female
/ Gene Expression Regulation, Neoplastic
/ Humans
/ Lungs
/ Mice
/ Neutrophil extracellular traps
/ Oncology
/ Proteins
/ Proto-Oncogene Proteins c-fos - genetics
/ Proto-Oncogene Proteins c-fos - metabolism
/ Triple Negative Breast Neoplasms - genetics
/ Triple Negative Breast Neoplasms - immunology
/ Triple Negative Breast Neoplasms - metabolism
/ Triple Negative Breast Neoplasms - pathology
/ Triple-negative breast cancer
/ Tumors
