ChemoNETosis: A road to tumor therapeutic resistance
Phei Er Saw1, Jianing Chen2, Erwei Song3
1Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Guangdong-Hong Kong Joint Laboratory for RNA Medicine, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, China.
Abstract:
Neutrophil extracellular traps (NETs) limit infection by trapping microorganisms and have recently been shown to induce tumor metastasis. In this issue of Cancer Cell, Mousset et al. illustrate how chemotherapy-induced inflammation confers chemoresistance by facilitating NETosis in malignant tumors, highlighting a therapeutic opportunity to target inflammatory NETs in cancer treatment.
Insights
Chemotherapy can trigger neutrophil extracellular traps (NETs), a form of cell death that promotes tumor growth and chemoresistance. Targeting these inflammatory NETs offers a new strategy for cancer treatment.
Area of Science:
- Oncology
- Immunology
- Cell Biology
Background:
- Neutrophil extracellular traps (NETs) are involved in infection control.
- Recent findings suggest NETs contribute to tumor metastasis.
- The role of NETs in chemotherapy response is not fully understood.
Purpose of the Study:
- To investigate the role of chemotherapy-induced inflammation in cancer treatment.
- To elucidate the mechanism by which NETs affect chemoresistance.
- To identify therapeutic targets within the NETosis pathway.
Main Methods:
- Utilized mouse models of malignant tumors.
- Analyzed the impact of chemotherapy on NET formation.
- Assessed the correlation between NETosis and tumor chemoresistance.
Main Results:
- Chemotherapy induces inflammation that promotes NETosis in tumors.
- NETosis was found to confer resistance to chemotherapy.
- Targeting inflammatory NETs presents a potential therapeutic strategy.
Conclusions:
- Chemotherapy-induced inflammation and NETosis contribute to chemoresistance.
- NETs represent a druggable target for improving cancer therapy outcomes.
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