- Titel
- Inflammation-Associated Cytotoxic Agents in Tumorigenesis
- Zitierfähige Url:
- https://nbn-resolving.org/urn:nbn:de:bsz:15-qucosa2-1007655
- Quellenangabe
- Cancers
Erscheinungsjahr: 2024
Jahrgang: 16
Heft: 1
E-ISSN: 2072-6694
Artikelnummer: 81 - Erstveröffentlichung
- 2024
- Abstract (EN)
- Chronic inflammatory processes are related to all stages of tumorigenesis. As inflammation is closely associated with the activation and release of different cytotoxic agents, the interplay between cytotoxic agents and antagonizing principles is highlighted in this review to address the question of how tumor cells overcome the enhanced values of cytotoxic agents in tumors. In tumor cells, the enhanced formation of mitochondrial-derived reactive species and elevated values of iron ions and free heme are antagonized by an overexpression of enzymes and proteins, contributing to the antioxidative defense and maintenance of redox homeostasis. Through these mechanisms, tumor cells can even survive additional stress caused by radio- and chemotherapy. Through the secretion of active agents from tumor cells, immune cells are suppressed in the tumor microenvironment and an enhanced formation of extracellular matrix components is induced. Different oxidant- and protease-based cytotoxic agents are involved in tumor-mediated immunosuppression, tumor growth, tumor cell invasion, and metastasis. Considering the special metabolic conditions in tumors, the main focus here was directed on the disturbed balance between the cytotoxic agents and protective mechanisms in late-stage tumors. This knowledge is mandatory for the implementation of novel anti-cancerous therapeutic approaches.
- Andere Ausgabe
- Erstveröffentlichung
DOI: 10.3390/cancers16010081 - Freie Schlagwörter (EN)
- cytotoxic agents, antagonizing principles, chronic inflammation, hypoxia, tumor cells, tumor microenvironment, immunosuppression, redox homeostasis, matrix remodeling
- Klassifikation (DDC)
- 610
- Verlag
- MDPI, Basel
- Version / Begutachtungsstatus
- publizierte Version / Verlagsversion
- URN Qucosa
- urn:nbn:de:bsz:15-qucosa2-1007655
- Veröffentlichungsdatum Qucosa
- 03.12.2025
- Dokumenttyp
- Artikel
- Sprache des Dokumentes
- Englisch
- Lizenz / Rechtehinweis
CC BY 4.0