Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Difference between revisions of "Karavyraki 2022 MitoFit"

From Bioblast
Line 3: Line 3:
{{Publication
{{Publication
|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
|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
|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.pdf A comparison of bioenergetics in human tongue pre-cancerous dysplastic oral keratinocytes and squamous cancer cells]
|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]
|authors=Karavyraki Marilena, Gnaiger Erich, Porter Richard K
|authors=Karavyraki Marilena, Gnaiger Erich, Porter Richard K
|year=2022-06-02
|year=2022-06-02
Line 9: Line 9:
|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
|mipnetlab=AT Innsbruck Oroboros, IE Dublin Porter RK
}}
}}
Karavyraki Marilena, [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-3647-5895]] Gnaiger Erich, [[File:ORCID.png|20px|link=https://orcid.org/0000-0001-9854-5161]] Porter Richard K
Karavyraki Marilena, [[File:ORCID.png|20px|link=https://orcid.org/0000-0003-3647-5895]] Gnaiger Erich, [[File:ORCID.png|20px|link=https://orcid.org/0000-0001-9854-5161]] Porter Richard K

Revision as of 07:41, 28 June 2022

Bioblast2022 banner.jpg


MitoFit Preprints         MitoFit Preprints        
Gnaiger 2019 MitoFit Preprints
       
Gnaiger MitoFit Preprints 2020.4
        MitoFit DOI Data Center         MitoPedia: Preprints         Bioenergetics Communications


Karavyraki 2022 MitoFit

Publications in the MiPMap
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

Β» MitoFit Preprints 2022.22.

MitoFit pdf

A comparison of bioenergetics in human tongue pre-cancerous dysplastic oral keratinocytes and squamous cancer cells

Karavyraki Marilena, Gnaiger Erich, Porter Richard K (2022-06-02) 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.


β€’ O2k-Network Lab: AT Innsbruck Oroboros, IE Dublin Porter RK

Karavyraki Marilena, ORCID.png Gnaiger Erich, ORCID.png 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