Cancer Letters, Journal Year: 2024, Volume and Issue: 592, P. 216903 - 216903
Published: April 24, 2024
Language: Английский
Cancer Letters, Journal Year: 2024, Volume and Issue: 592, P. 216903 - 216903
Published: April 24, 2024
Language: Английский
Cell, Journal Year: 2024, Volume and Issue: 187(7), P. 1589 - 1616
Published: March 1, 2024
Language: Английский
Citations
161Cancer Cell, Journal Year: 2023, Volume and Issue: 41(4), P. 757 - 775.e10
Published: April 1, 2023
Language: Английский
Citations
121Cancer Cell, Journal Year: 2024, Volume and Issue: 42(3), P. 474 - 486.e12
Published: Feb. 22, 2024
Language: Английский
Citations
72Annual Review of Pathology Mechanisms of Disease, Journal Year: 2024, Volume and Issue: 19(1), P. 227 - 259
Published: Jan. 24, 2024
Infections, cardiovascular disease, and cancer are major causes of disease death worldwide. Neutrophils inescapably associated with each these health concerns, by either protecting from, instigating, or aggravating their impact on the host. However, disorders has a very different etiology, understanding how neutrophils contribute to them requires intricacies this immune cell type, including nonimmune contributions physiology pathology. Here, we review some intricacies, from basic concepts in neutrophil biology, such as production acquisition functional diversity, variety mechanisms which they preventing infections, events, cancer. We also poorly explored aspects promote favoring tissue repair discuss discoveries about biology inform development new therapeutic strategies.
Language: Английский
Citations
39Signal Transduction and Targeted Therapy, Journal Year: 2024, Volume and Issue: 9(1)
Published: Sept. 20, 2024
Language: Английский
Citations
29Journal of Clinical Investigation, Journal Year: 2024, Volume and Issue: 134(5)
Published: Jan. 9, 2024
Neutrophil Extracellular Traps (NETs), a web-like structure of cytosolic and granule proteins assembled on decondensed chromatin, kill pathogens causes tissue damage in diseases. Whether NETs can cancer cells is unexplored. Here, we report that combination glutaminase inhibitor CB-839 5-FU inhibits the growth PIK3CA mutant colorectal cancers (CRCs) xenograft, syngeneic, genetically engineered mouse models part through NETs. Disruption by either DNase I treatment or depletion neutrophils CRCs attenuated efficacy drug combination. Moreover, were present tumor biopsies taken from patients treated with phase II clinical trial. Increased NET levels tumors are associated longer progression-free survival. Mechanistically, induced expression IL-8 preferentially to attract into tumors. Further, increased reactive oxygen species neutrophils, thereby inducing Cathepsin G (CTSG), serine protease localized NETs, enters CRC RAGE cell surface protein. The internalized CTSG cleaves 14-3-3 proteins, releases Bax, triggers apoptosis cells. Thus, our studies illuminate previously unrecognized mechanism which chemotherapy-induced
Language: Английский
Citations
28Oncogene, Journal Year: 2024, Volume and Issue: unknown
Published: March 12, 2024
Language: Английский
Citations
24Immunity & Ageing, Journal Year: 2024, Volume and Issue: 21(1)
Published: June 14, 2024
Abstract Alzheimer’s disease (AD) is a serious brain disorder characterized by the presence of beta-amyloid plaques, tau pathology, inflammation, neurodegeneration, and cerebrovascular dysfunction. The chronic neuroinflammation, breaches in blood-brain barrier (BBB), increased levels inflammatory mediators are central to pathogenesis AD. These factors promote penetration immune cells into brain, potentially exacerbating clinical symptoms neuronal death AD patients. While microglia, resident nervous system (CNS), play crucial role AD, recent evidence suggests infiltration cerebral vessels parenchyma peripheral cells, including neutrophils, T lymphocytes, B NK monocytes participate regulation immunity which expected huge future immunotherapy. Given this article seeks offer comprehensive overview their contributions neuroinflammation disease. Understanding these neuroinflammatory response vital for developing new diagnostic markers therapeutic targets enhance diagnosis treatment
Language: Английский
Citations
16Clinical and Translational Medicine, Journal Year: 2025, Volume and Issue: 15(2)
Published: Jan. 26, 2025
Abstract To investigate the potential mechanisms underlying neutrophil extracellular traps (NETs) confer ferroptosis resistance and CD8(+) T cell inhibition in lung adenocarcinoma (LUAD). By intravenous injection of LLC cells into tail vein, a LUAD mouse model was created. Phorbol‐12‐myristate‐13‐acetate (PMA) stimulated neutrophils to facilitate NETs formation combined with inhibitor DNase I explore mechanism on proliferation, migration, resistance, activity. CitH3, myeloperoxidase (MPO), cell‐free DNA, MPO‐DNA levels were increased, indicating an increase LUAD. PMA promoted tumours mice, increased number CD3(+)CD4(+) cells, decreased perforin, granzyme A, B, IFNγ, TNF‐α levels, growth tumour nodules, that formation, reduced activity CD8(+)T growth. partially reversed effects PMA. proliferation while effects. Erastin inhibited migration ferroptosis. Further results showed by promoting YTHDF2‐mediated SLC2A3 mRNA degradation. Sh‐YTHDF2 effect whereas si‐SLC2A3 sh‐YTHDF2 cells. In addition, inhibiting tumours, Our suggested through
Language: Английский
Citations
3Nature Immunology, Journal Year: 2025, Volume and Issue: 26(1), P. 17 - 28
Published: Jan. 1, 2025
Language: Английский
Citations
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