Difference between revisions of "Smolkova 2010 J Bioenerg Biomembr"
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{{Publication | {{Publication | ||
|title=Smolková K, Bellance N, Scandurra F, Génot E, Gnaiger E, Plecitá-Hlavatá L, Ježek P, Rossignol R (2010) Mitochondrial bioenergetic adaptations of breast cancer cells to aglycemia and hypoxia. J Bioenerg Biomembr 42:55-67. | |title=Smolková K, Bellance N, Scandurra F, Génot E, Gnaiger E, Plecitá-Hlavatá L, Ježek P, Rossignol R (2010) Mitochondrial bioenergetic adaptations of breast cancer cells to aglycemia and hypoxia. https://doi.org/10.1007/s10863-009-9267-x | ||
|info=J Bioenerg Biomembr 42:55-67. [http://www.ncbi.nlm.nih.gov/pubmed/20084539 PMID: 20084539]»[[File:O2k-brief.png|36px|link=http://wiki.oroboros.at/images/b/b7/Smolkova_2010_J_Bioenerg_Biomembr_O2k-brief.pdf|O2k-brief]] | |||
|authors=Smolkova K, Bellance N, Scandurra FM, Genot E, Gnaiger | |authors=Smolkova K, Bellance N, Scandurra FM, Genot E, Gnaiger Erich, Plecita-Hlavata L, Jezek P, Rossignol R | ||
|year=2010 | |year=2010 | ||
|journal=J Bioenerg Biomembr | |journal=J Bioenerg Biomembr | ||
|abstract=Breast cancer cells can survive and proliferate under harsh conditions of nutrient deprivation, including limited oxygen and glucose availability. We hypothesized that such environments trigger metabolic adaptations of mitochondria, which promote tumor progression. Here, we mimicked aglycemia and hypoxia ''in vitro'' and compared the mitochondrial and cellular bioenergetic adaptations of human breast cancer (HTB-126) and non-cancer (HTB-125) cells that originate from breast tissue. Using high-resolution respirometry and western blot analyses, we demonstrated that 4 days of glucose deprivation elevated oxidative phosphorylation five-fold, increased the spread of the mitochondrial network without changing its shape, and decreased the apparent affinity of oxygen in cancer cells (increase in | |abstract=[[Image:O2k-Publications.jpg|80px|link=O2k-Publications: Topics|O2k-Publications: Topics]] | ||
Breast cancer cells can survive and proliferate under harsh conditions of nutrient deprivation, including limited oxygen and glucose availability. We hypothesized that such environments trigger metabolic adaptations of mitochondria, which promote tumor progression. Here, we mimicked aglycemia and hypoxia ''in vitro'' and compared the mitochondrial and cellular bioenergetic adaptations of human breast cancer (HTB-126) and non-cancer (HTB-125) cells that originate from breast tissue. Using high-resolution respirometry and western blot analyses, we demonstrated that 4 days of glucose deprivation elevated oxidative phosphorylation five-fold, increased the spread of the mitochondrial network without changing its shape, and decreased the apparent affinity of oxygen in cancer cells (increase in ''c''<sub>50</sub>), whereas it remained unchanged in control cells. The substrate control ratios also remained constant following adaptation. We also observed the Crabtree effect, specifically in HTB-126 cells. Likewise, sustained hypoxia (1% oxygen during 6 days) improved cell respiration in non-cancer cells grown in glucose or glucose-deprived medium (+ 32% and +38%, respectively). Conversely, under these conditions of limited oxygen or a combination of oxygen and glucose deprivation for 6 days, routine respiration was strongly reduced in cancer cells (-36% in glucose medium, -24% in glucose-deprived medium). The data demonstrate that cancer cells behave differently than normal cells when adapting their bioenergetics to microenvironmental conditions. The differences in hypoxia and aglycemia tolerance between breast cancer cells and non-cancer cells may be important when optimizing strategies for the treatment of breast cancer. | |||
|keywords=Mitochondria, Oxidative phosphorylation, Breast cancer, Tumor bioenergetics, Hypoxia, Respirometry | |keywords=Mitochondria, Oxidative phosphorylation, Breast cancer, Tumor bioenergetics, Hypoxia, Respirometry | ||
|mipnetlab=AT Innsbruck Gnaiger E, CZ Prague Jezek P, FR Bordeaux Rossignol R | |mipnetlab=AT Innsbruck Gnaiger E, CZ Prague Jezek P, FR Bordeaux Rossignol R | ||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} | ||
[[File:O2k-brief.png|36px|left]] | |||
== O2k-brief == | |||
::::» [[O2k-brief |List of O2k-Publications presented as O2k-brief]] | |||
== O2k-Publications == | |||
::::* [[O2k-Publications: Cancer]] | |||
== Cited by == | |||
::* 39 articles in PubMed (2021-12-27) https://pubmed.ncbi.nlm.nih.gov/20084539/ | |||
{{Labeling | {{Labeling | ||
|area=Respiration, mt-Biogenesis;mt-density | |area=Respiration, mt-Biogenesis;mt-density | ||
|diseases=Cancer | |||
|organism=Human | |organism=Human | ||
| | |tissues=Fibroblast | ||
|preparations=Intact cells | |preparations=Intact cells | ||
|topics=Oxygen kinetics | |||
|topics= | |couplingstates=ROUTINE, OXPHOS, ET | ||
|couplingstates=ROUTINE, OXPHOS, | |pathways=N, NS | ||
| | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
|additional=O2k-brief | |||
}} | }} | ||
Latest revision as of 13:57, 12 June 2022
| Smolková K, Bellance N, Scandurra F, Génot E, Gnaiger E, Plecitá-Hlavatá L, Ježek P, Rossignol R (2010) Mitochondrial bioenergetic adaptations of breast cancer cells to aglycemia and hypoxia. https://doi.org/10.1007/s10863-009-9267-x |
» J Bioenerg Biomembr 42:55-67. PMID: 20084539»
Smolkova K, Bellance N, Scandurra FM, Genot E, Gnaiger Erich, Plecita-Hlavata L, Jezek P, Rossignol R (2010) J Bioenerg Biomembr
Abstract: 
Breast cancer cells can survive and proliferate under harsh conditions of nutrient deprivation, including limited oxygen and glucose availability. We hypothesized that such environments trigger metabolic adaptations of mitochondria, which promote tumor progression. Here, we mimicked aglycemia and hypoxia in vitro and compared the mitochondrial and cellular bioenergetic adaptations of human breast cancer (HTB-126) and non-cancer (HTB-125) cells that originate from breast tissue. Using high-resolution respirometry and western blot analyses, we demonstrated that 4 days of glucose deprivation elevated oxidative phosphorylation five-fold, increased the spread of the mitochondrial network without changing its shape, and decreased the apparent affinity of oxygen in cancer cells (increase in c50), whereas it remained unchanged in control cells. The substrate control ratios also remained constant following adaptation. We also observed the Crabtree effect, specifically in HTB-126 cells. Likewise, sustained hypoxia (1% oxygen during 6 days) improved cell respiration in non-cancer cells grown in glucose or glucose-deprived medium (+ 32% and +38%, respectively). Conversely, under these conditions of limited oxygen or a combination of oxygen and glucose deprivation for 6 days, routine respiration was strongly reduced in cancer cells (-36% in glucose medium, -24% in glucose-deprived medium). The data demonstrate that cancer cells behave differently than normal cells when adapting their bioenergetics to microenvironmental conditions. The differences in hypoxia and aglycemia tolerance between breast cancer cells and non-cancer cells may be important when optimizing strategies for the treatment of breast cancer. • Keywords: Mitochondria, Oxidative phosphorylation, Breast cancer, Tumor bioenergetics, Hypoxia, Respirometry
• O2k-Network Lab: AT Innsbruck Gnaiger E, CZ Prague Jezek P, FR Bordeaux Rossignol R
O2k-brief
O2k-Publications
Cited by
- 39 articles in PubMed (2021-12-27) https://pubmed.ncbi.nlm.nih.gov/20084539/
Labels: MiParea: Respiration, mt-Biogenesis;mt-density
Pathology: Cancer
Organism: Human Tissue;cell: Fibroblast Preparation: Intact cells
Regulation: Oxygen kinetics Coupling state: ROUTINE, OXPHOS, ET Pathway: N, NS HRR: Oxygraph-2k
O2k-brief
