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Caveolin-1 in oncogenic metabolic symbiosis
M. Raudenska, J. Gumulec, J. Balvan, M. Masarik
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
32196654
DOI
10.1002/ijc.32987
Knihovny.cz E-resources
- MeSH
- Caveolin 1 metabolism MeSH
- Humans MeSH
- Cell Communication MeSH
- Tumor Microenvironment MeSH
- Neoplasms metabolism MeSH
- Gene Expression Regulation, Neoplastic MeSH
- Symbiosis MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
Metabolic phenotypes of cancer cells are heterogeneous and flexible as a tumor mass is a hurriedly evolving system capable of constant adaptation to oxygen and nutrient availability. The exact type of cancer metabolism arises from the combined effects of factors intrinsic to the cancer cells and factors proposed by the tumor microenvironment. As a result, a condition termed oncogenic metabolic symbiosis in which components of the tumor microenvironment (TME) promote tumor growth often occurs. Understanding how oncogenic metabolic symbiosis emerges and evolves is crucial for perceiving tumorigenesis. The process by which tumor cells reprogram their TME involves many mechanisms, including changes in intercellular communication, alterations in metabolic phenotypes of TME cells, and rearrangement of the extracellular matrix. It is possible that one molecule with a pleiotropic effect such as Caveolin-1 may affect many of these pathways. Here, we discuss the significance of Caveolin-1 in establishing metabolic symbiosis in TME.
BIOCEV 1st Faculty of Medicine Charles University Vestec Czech Republic
Department of Chemistry and Biochemistry Mendel University in Brno Brno Czech Republic
Department of Pathological Physiology Faculty of Medicine Masaryk University Brno Czech Republic
Department of Physiology Faculty of Medicine Masaryk University Brno Czech Republic
References provided by Crossref.org
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