dc.contributor.author | Dong, Lanfeng | |
dc.contributor.author | Neuzil, Jiri | |
dc.date.accessioned | 2019-11-04T04:59:21Z | |
dc.date.available | 2019-11-04T04:59:21Z | |
dc.date.issued | 2019 | |
dc.identifier.issn | 2523-3548 | |
dc.identifier.doi | 10.1186/s40880-019-0412-6 | |
dc.identifier.uri | http://hdl.handle.net/10072/388890 | |
dc.description.abstract | Mitochondria are organelles controlling adenosine triphosphate (ATP) generation, redox homeostasis, metabolic signaling, and apoptotic pathways. Although glycolysis was traditionally considered as the major source of energy in cancer cells, in-line with the so-called “Warburg effect”, mitochondria have been recognized to play a key role in oncogenesis [1]. Cancer cells uniquely reprogram their cellular activities to support their rapid proliferation and migration, as well as to counteract metabolic and genotoxic stress during cancer progression [2]. Further, mitochondria can switch their metabolic phenotypes to meet the challenges of high energy demand and macromolecular synthesis [3]. Thus, cancer mitochondria have the ability to flexibly switching between glycolysis and oxidative phosphorylation (OXPHOS) for their survival. The electron transport chain (ETC) function is pivotal for mitochondrial respiration, which is also needed for dihydroorotate dehydrogenase (DHODH) activity that is essential for de novo pyrimidine synthesis [4]. Recent researches have demonstrated that cancer cells devoid of mitochondrial DNA (mtDNA) lack their tumorigenic potential, and they re-gain this ability by acquiring healthy mtDNA from the host stromal cells via horizontal transfer of whole mitochondria [5, 6] for recovery of the respiratory function. Functionally, respiration propels DHODH activity for pyrimidine biosynthesis [7]. Therefore, targeting mitochondria holds great potential for anticancer strategy with high therapeutic opportunities. | |
dc.description.peerreviewed | Yes | |
dc.language | English | |
dc.language.iso | eng | |
dc.publisher | BioMed Central Ltd. | |
dc.publisher.place | United Kingdom | |
dc.relation.ispartofpagefrom | 63: 1 | |
dc.relation.ispartofpageto | 63: 3 | |
dc.relation.ispartofissue | 1 | |
dc.relation.ispartofjournal | Cancer Communications | |
dc.relation.ispartofvolume | 39 | |
dc.subject.fieldofresearch | Oncology and carcinogenesis | |
dc.subject.fieldofresearchcode | 3211 | |
dc.title | Targeting mitochondria as an anticancer strategy | |
dc.type | Journal article | |
dc.type.description | C2 - Articles (Other) | |
dcterms.bibliographicCitation | Dong, L; Neuzil, J, Targeting mitochondria as an anticancer strategy, Cancer Communications, 2019, 39 (1), pp. 63: 1-63: 3 | |
dcterms.license | http://creativecommons.org/licenses/by/4.0/ | |
dc.date.updated | 2019-10-31T01:48:48Z | |
dc.description.version | Version of Record (VoR) | |
gro.rights.copyright | © The Author(s) 2019. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creat iveco mmons .org/licen ses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. | |
gro.hasfulltext | Full Text | |
gro.griffith.author | Neuzil, Jiri | |