Targeting of stress response pathways in the prevention and treatment of cancer
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
29339119
DOI
10.1016/j.biotechadv.2018.01.007
PII: S0734-9750(18)30007-7
Knihovny.cz E-resources
- Keywords
- AMPK, Cancer, HIF1α, HO-1, Metabolism, Nrf2, Oxidative stress, PGC1α, Sirtuins,
- MeSH
- Antioxidants metabolism MeSH
- Autophagy MeSH
- Exercise MeSH
- Stress, Physiological physiology MeSH
- Hormesis MeSH
- Caloric Restriction MeSH
- Humans MeSH
- Mutagenesis MeSH
- Neoplasms etiology prevention & control therapy MeSH
- Oxidative Stress MeSH
- Polyphenols pharmacology MeSH
- Inflammation complications metabolism MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Antioxidants MeSH
- Polyphenols MeSH
The hallmarks of tumor tissue are not only genetic aberrations but also the presence of metabolic and oxidative stress as a result of hypoxia and lactic acidosis. The stress activates several prosurvival pathways including metabolic remodeling, autophagy, antioxidant response, mitohormesis, and glutaminolysis, whose upregulation in tumors is associated with a poor survival of patients, while their activation in healthy tissue with statins, metformin, physical activity, and natural compounds prevents carcinogenesis. This review emphasizes the dual role of stress response pathways in cancer and suggests the integrative understanding as a basis for the development of rational therapy targeting the stress response.
References provided by Crossref.org
Postbiotics, Metabolic Signaling, and Cancer
