Energy and Redox Homeostasis in Tumor Cells
Cancer cells display abnormal morphology, chromosomes, and metabolism. This review will focus on the metabolism of tumor cells integrating the available data by way of a functional approach. The first part contains a comprehensive introduction to bioenergetics, mitochondria, and the mechanisms of pr...
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| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
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Wiley
2012-01-01
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| Series: | International Journal of Cell Biology |
| Online Access: | http://dx.doi.org/10.1155/2012/593838 |
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| _version_ | 1850106486179495936 |
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| author | Marcus Fernandes de Oliveira Nívea Dias Amoêdo Franklin David Rumjanek |
| author_facet | Marcus Fernandes de Oliveira Nívea Dias Amoêdo Franklin David Rumjanek |
| author_sort | Marcus Fernandes de Oliveira |
| collection | DOAJ |
| description | Cancer cells display abnormal morphology, chromosomes, and metabolism. This review will focus on the metabolism of tumor cells integrating the available data by way of a functional approach. The first part contains a comprehensive introduction to bioenergetics, mitochondria, and the mechanisms of production and degradation of reactive oxygen species. This will be followed by a discussion on the oxidative metabolism of tumor cells including the morphology, biogenesis, and networking of mitochondria. Tumor cells overexpress proteins that favor fission, such as GTPase dynamin-related protein 1 (Drp1). The interplay between proapoptotic members of the Bcl-2 family that promotes Drp 1-dependent mitochondrial fragmentation and fusogenic antiapoptotic proteins such as Opa-1 will be presented. It will be argued that contrary to the widespread belief that in cancer cells, aerobic glycolysis completely replaces oxidative metabolism, a misrepresentation of Warburg’s original results, mitochondria of tumor cells are fully viable and functional. Cancer cells also carry out oxidative metabolism and generally conform to the orthodox model of ATP production maintaining as well an intact electron transport system. Finally, data will be presented indicating that the key to tumor cell survival in an ROS rich environment depends on the overexpression of antioxidant enzymes and high levels of the nonenzymatic antioxidant scavengers. |
| format | Article |
| id | doaj-art-2e42ab7c368042d68c0427fa3efa9126 |
| institution | OA Journals |
| issn | 1687-8876 1687-8884 |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Cell Biology |
| spelling | doaj-art-2e42ab7c368042d68c0427fa3efa91262025-08-20T02:38:49ZengWileyInternational Journal of Cell Biology1687-88761687-88842012-01-01201210.1155/2012/593838593838Energy and Redox Homeostasis in Tumor CellsMarcus Fernandes de Oliveira0Nívea Dias Amoêdo1Franklin David Rumjanek2Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Cidade Universitária, 21941-970 Rio de Janeiro, RJ, BrazilInstituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Cidade Universitária, 21941-970 Rio de Janeiro, RJ, BrazilInstituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Cidade Universitária, 21941-970 Rio de Janeiro, RJ, BrazilCancer cells display abnormal morphology, chromosomes, and metabolism. This review will focus on the metabolism of tumor cells integrating the available data by way of a functional approach. The first part contains a comprehensive introduction to bioenergetics, mitochondria, and the mechanisms of production and degradation of reactive oxygen species. This will be followed by a discussion on the oxidative metabolism of tumor cells including the morphology, biogenesis, and networking of mitochondria. Tumor cells overexpress proteins that favor fission, such as GTPase dynamin-related protein 1 (Drp1). The interplay between proapoptotic members of the Bcl-2 family that promotes Drp 1-dependent mitochondrial fragmentation and fusogenic antiapoptotic proteins such as Opa-1 will be presented. It will be argued that contrary to the widespread belief that in cancer cells, aerobic glycolysis completely replaces oxidative metabolism, a misrepresentation of Warburg’s original results, mitochondria of tumor cells are fully viable and functional. Cancer cells also carry out oxidative metabolism and generally conform to the orthodox model of ATP production maintaining as well an intact electron transport system. Finally, data will be presented indicating that the key to tumor cell survival in an ROS rich environment depends on the overexpression of antioxidant enzymes and high levels of the nonenzymatic antioxidant scavengers.http://dx.doi.org/10.1155/2012/593838 |
| spellingShingle | Marcus Fernandes de Oliveira Nívea Dias Amoêdo Franklin David Rumjanek Energy and Redox Homeostasis in Tumor Cells International Journal of Cell Biology |
| title | Energy and Redox Homeostasis in Tumor Cells |
| title_full | Energy and Redox Homeostasis in Tumor Cells |
| title_fullStr | Energy and Redox Homeostasis in Tumor Cells |
| title_full_unstemmed | Energy and Redox Homeostasis in Tumor Cells |
| title_short | Energy and Redox Homeostasis in Tumor Cells |
| title_sort | energy and redox homeostasis in tumor cells |
| url | http://dx.doi.org/10.1155/2012/593838 |
| work_keys_str_mv | AT marcusfernandesdeoliveira energyandredoxhomeostasisintumorcells AT niveadiasamoedo energyandredoxhomeostasisintumorcells AT franklindavidrumjanek energyandredoxhomeostasisintumorcells |