ArticleCancer research2025
Surgery-Induced Neutrophil Extracellular Traps Promote Tumor Metastasis by Reprogramming Cancer Cell Lipid Metabolism.
Article in Cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Leveraging Microphysiological Systems to Facilitate Neutrophil-Based Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Reprogramming pulmonary B cells by ANXA1 silencing halts lung metastatic niche formation in breast cancer.Journal of nanobiotechnology · 2026Article
- MYC in Oncogenesis and Therapeutic Implications.MedComm · 2026Review
- Anoikis in cancer: molecular mechanisms, resistance, and therapeutic strategies.Apoptosis : an international journal on programmed cell death · 2026Review
- Guided immunotherapy for residual solid tumor: integrating platelets and CAR T cells to reduce post-surgical recurrence.Biomarker research · 2026Review
- Prognostic significance of intratumoral neutrophil extracellular traps in pulmonary pleomorphic carcinoma: comparison with adenocarcinoma.BJC reports · 2026Article
- A weakly supervised deep learning-based recurrence prediction and risk stratification of lung adenocarcinoma from pathology whole-slide images.BMC cancer · 2026Article
- Platelet-neutrophil cooperation in cancer: mechanisms of metastatic niche formation and implications for prognostic stratification and therapy.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Review
- Neutrophil Extracellular Traps in Cancer Metastasis: From Mechanistic Understanding to Targeted Therapy.Current oncology (Toronto, Ont.) · 2026Review
- Roles of anesthetics in modulating neutrophil extracellular traps formation: a review of current literature.Annals of medicine and surgery (2012) · 2026Article
- Metabolic Landscape of Endometrial Cancer: Insights into Pathway Dysregulation and Metabolic Features.Biomedicines · 2026Article
- Postoperative Abdominal Infectious Complications Promote Colon Cancer Metastasis by Inducing MDSCs to Release Neutrophil Extracellular Traps.Journal of inflammation research · 2026Article
- The immunosuppressive tumor microenvironment in glioblastoma.Frontiers in immunology · 2026Review
- Gut microbiota-innate immune crosstalk in the initiation and progression of CRC: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Effects of surgery on cancer metastasis: biological mechanisms and perioperative implications.Frontiers in oncology · 2026Review
- The OtR tumor recurrence and metastasis model reveals doxorubicin-induced tumor shrinkage doesn't guarantee prolonged survival.Animal models and experimental medicine · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
Cancer surgery is a double-edged sword, as it can induce an inflammatory response that promotes tumor recurrence and progression. In this study, we explored the effects of surgery-induced neutrophil extracellular traps (NET) in reprogramming cancer metabolism to foster metastatic tumor growth. To model the effect of surgery on tumor progression, mice bearing subcutaneous tumors underwent a midline laparotomy with mesenteric exploration for 30 minutes. Mice subjected to surgery showed accelerated primary subcutaneous and lung metastatic tumor growth. Perioperative inhibition of NET formation utilizing DNAse, GSK484, or peptidyl arginine deiminase 4 knockout mice prevented surgically induced tumor growth, whereas pretreating cancer cells with NETs in vitro before inoculation increased tumor burden. Cancer cells exposed to surgical stress in vivo or treated with NETs in vitro showed activation of the MYC oncogenic pathway and fatty acid (FA) oxidation (FAO). NETs also stimulated the uptake of long-chain FAs and upregulation of CD36, the main long-chain FA transporter. Blocking FAO with etomoxir, a carnitine palmitoyl transferase Iα inhibitor, prevented metastatic tumor growth induced by surgical NETs. FA metabolism was crucial for cancer cells under anoikis stress, allowing the survival of circulating cancer cells exposed to NETs. Analysis of patient data substantiated the correlation between NET abundance and lipid metabolism, and plasma from postoperative patients upregulated CD36 expression and promoted the proliferation of colorectal cancer cells. Together, these findings show that the systemic NETosis response triggered by surgery promotes tumor progression by activating the MYC transcriptional program and reprogramming FAO metabolism in cancer cells. SIGNIFICANCE: Surgery stimulates formation of neutrophil extracellular traps that promote fatty acid oxidation to support survival of disseminated cancer cells and metastasis, indicating that targeting this inflammation-metabolism axis may prevent tumor progression.
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