Karavyraki 2022 MitoFit: Difference between revisions
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|title=Karavyraki M, Gnaiger E, Porter RK (2022) A comparison of bioenergetics in human tongue pre-cancerous dysplastic oral keratinocytes and squamous cancer cells. https://doi.org/10.26124/mitofit:2022-0022 — ''2022-11-11 published in [https://doi.org//10.26124/bec:2022-0011 '''Bioenerg Commun 2022.11.''']'' | |title=Karavyraki M, Gnaiger E, Porter RK (2022) A comparison of bioenergetics in human tongue pre-cancerous dysplastic oral keratinocytes and squamous cancer cells. https://doi.org/10.26124/mitofit:2022-0022 — ''2022-11-11 published in [https://doi.org//10.26124/bec:2022-0011 '''Bioenerg Commun 2022.11.''']'' | ||
|info=MitoFit Preprints 2022.22. [[File:MitoFit Preprints pdf.png|left|160px|link=https://wiki.oroboros.at/images/0/0a/Karavyraki_2022_MitoFit.pdf|MitoFit pdf]] [https://wiki.oroboros.at/images/0/0a/Karavyraki_2022_MitoFit.pdf A comparison of bioenergetics in human tongue pre-cancerous dysplastic oral keratinocytes and squamous cancer cells] [[File:WatchThePresentationYoutube_icon.jpg|200px|link=https://www.youtube.com/watch?v=GyS9ePicMlg&t=1925s|»''Watch the presentation''«]] | |info=MitoFit Preprints 2022.22. [[File:MitoFit Preprints pdf.png|left|160px|link=https://wiki.oroboros.at/images/0/0a/Karavyraki_2022_MitoFit.pdf|MitoFit pdf]] [https://wiki.oroboros.at/images/0/0a/Karavyraki_2022_MitoFit.pdf A comparison of bioenergetics in human tongue pre-cancerous dysplastic oral keratinocytes and squamous cancer cells] [[File:WatchThePresentationYoutube_icon.jpg|200px|link=https://www.youtube.com/watch?v=GyS9ePicMlg&t=1925s|»''Watch the presentation''«]] | ||
|year=2022 | |authors=MitoFit Prep 2022.22. | ||
|year=2022 | |||
|journal=MitoFit Prep | |journal=MitoFit Prep | ||
|abstract=[[Porter 2022 Abstract Bioblast]]: In an endeavour to understand the metabolic phenotype behind oral squamous cell carcinomas, we characterised the bioenergetic profile of a human tongue derived cancer cell line (SCC-4 cells) and compared this profile to a pre-cancerous dysplastic oral keratinocyte (DOK) cell line also derived from human tongue. The human SCC-4 cancer cells had greater mitochondrial densitydensity but lower mitochondrial O2 flow per cell than DOK cells. The lower oxygen consumption rate in SCC-4 cells can be partially explained by lower NADH-related enzymatic activity and lower mitochondrial Complex I activity when compared to pre-cancerous DOK cells. In addition, SCC-4 cells have greater extracellular acidification rate (an index of glycolytic flux) when compared to DOK cells. In addition, treatment with recombinant human IL-6 (rhIL-6), known to drive anoikis resistance in SCC-4 cells but not DOK cells, impairs oxygen consumption in SCC-4 but not DOK cells, without affecting mitochondrial density. We conclude that SCC-4 cells have a less oxidative phenotype compared to DOK cells and that IL-6 attenuates mitochondrial function in SCC-4 cells while increasing glycolytic flux. | |abstract=[[Porter 2022 Abstract Bioblast]]: In an endeavour to understand the metabolic phenotype behind oral squamous cell carcinomas, we characterised the bioenergetic profile of a human tongue derived cancer cell line (SCC-4 cells) and compared this profile to a pre-cancerous dysplastic oral keratinocyte (DOK) cell line also derived from human tongue. The human SCC-4 cancer cells had greater mitochondrial densitydensity but lower mitochondrial O2 flow per cell than DOK cells. The lower oxygen consumption rate in SCC-4 cells can be partially explained by lower NADH-related enzymatic activity and lower mitochondrial Complex I activity when compared to pre-cancerous DOK cells. In addition, SCC-4 cells have greater extracellular acidification rate (an index of glycolytic flux) when compared to DOK cells. In addition, treatment with recombinant human IL-6 (rhIL-6), known to drive anoikis resistance in SCC-4 cells but not DOK cells, impairs oxygen consumption in SCC-4 but not DOK cells, without affecting mitochondrial density. We conclude that SCC-4 cells have a less oxidative phenotype compared to DOK cells and that IL-6 attenuates mitochondrial function in SCC-4 cells while increasing glycolytic flux. | ||
|mipnetlab=AT Innsbruck Oroboros, IE Dublin Porter RK | |mipnetlab=AT Innsbruck Oroboros, IE Dublin Porter RK | ||
}} | }} | ||
Latest revision as of 12:38, 8 January 2023
Karavyraki 2022 MitoFit
| Karavyraki M, Gnaiger E, Porter RK (2022) A comparison of bioenergetics in human tongue pre-cancerous dysplastic oral keratinocytes and squamous cancer cells. https://doi.org/10.26124/mitofit:2022-0022 — 2022-11-11 published in Bioenerg Commun 2022.11. |
» MitoFit Preprints 2022.22.
MitoFit Prep 2022.22. (2022) MitoFit Prep
Abstract: Porter 2022 Abstract Bioblast: In an endeavour to understand the metabolic phenotype behind oral squamous cell carcinomas, we characterised the bioenergetic profile of a human tongue derived cancer cell line (SCC-4 cells) and compared this profile to a pre-cancerous dysplastic oral keratinocyte (DOK) cell line also derived from human tongue. The human SCC-4 cancer cells had greater mitochondrial densitydensity but lower mitochondrial O2 flow per cell than DOK cells. The lower oxygen consumption rate in SCC-4 cells can be partially explained by lower NADH-related enzymatic activity and lower mitochondrial Complex I activity when compared to pre-cancerous DOK cells. In addition, SCC-4 cells have greater extracellular acidification rate (an index of glycolytic flux) when compared to DOK cells. In addition, treatment with recombinant human IL-6 (rhIL-6), known to drive anoikis resistance in SCC-4 cells but not DOK cells, impairs oxygen consumption in SCC-4 but not DOK cells, without affecting mitochondrial density. We conclude that SCC-4 cells have a less oxidative phenotype compared to DOK cells and that IL-6 attenuates mitochondrial function in SCC-4 cells while increasing glycolytic flux.
• O2k-Network Lab: AT Innsbruck Oroboros, IE Dublin Porter RK
Karavyraki Marilena, 
Gnaiger Erich, Porter Richard K
Data availability
- All data will be available.
Support
- Marie Curie Grant TRACT 721906 H2020-MCSA-ITN 2016; COST Action CA15203 MitoEAGLE (2016-2021). We thank Rafael Moreno-Sanchez for a constructive review of our manuscript.
Labels: MiParea: Respiration
Pathology: Cancer
Organism: Human
Preparation: Permeabilized cells Enzyme: Complex I, Marker enzyme, TCA cycle and matrix dehydrogenases Regulation: Aerobic glycolysis Coupling state: LEAK, ROUTINE, ET Pathway: S, ROX HRR: Oxygraph-2k
Bioblast 2022, Crabtree effect
