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Difference between revisions of "Porter 2022 Abstract Bioblast"

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[[File:Bioblast2022 banner.jpg|link=Bioblast_2022]]
{{Abstract
{{Abstract
|title=Karavyraki M, Gnaiger E, Porter RK (2022) A comparison of bioenergetics in human tongue pre-cancerous dysplastic oral keratinocytes and squamous cancer cells. Bioblast 2022: BEC Inaugural Conference.
|title=[[File:Richie.jpg|left|100px|Porter Richard K]] Karavyraki M, Gnaiger E, <u>Porter Richard K</u> (2022) A comparison of bioenergetics in human tongue pre-cancerous dysplastic oral keratinocytes and squamous cancer cells. Bioblast 2022: BEC Inaugural Conference.
|info=[https://wiki.oroboros.at/index.php/Bioblast_2022#Submitted_abstracts Bioblast 2022: BEC Inaugural Conference]
|info=[https://wiki.oroboros.at/index.php/Bioblast_2022#Submitted_abstracts Bioblast 2022: BEC Inaugural Conference]
|authors=Karavyraki Marilena, Gnaiger Erich, Porter Richard K
|authors=Karavyraki Marilena, Gnaiger Erich, Porter Richard K
|year=2022
|year=2022
|event=Bioblast 2022
|event=Bioblast 2022
|abstract=In an endeavour to understand the metabolic phenotype behind metastasis from 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 abundance but lower mitochondrial oxygen consumption rates than DOK cells. The lower oxygen consumption rate in SCC-4 cells can be partially explained by lower NADH-related enzymatic 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 abundance. 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=In an endeavour to understand the metabolic phenotype behind metastasis from 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 density but lower mitochondrial O<sub>2</sub> flow per cell ''J''<sub>O<sub>2</sub></sub> than DOK cells. The lower cell ''J''<sub>O<sub>2</sub></sub> in SCC-4 cells can be partially explained by lower NADH-related enzymatic 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 
|keywords=Oral Squamous Cancer Cells, Mitochondria, Interleukin 6, Dysplastic oral keratinocytes, Oxygen consumption
|keywords=Oral Squamous Cancer Cells, Mitochondria, Interleukin 6, Dysplastic oral keratinocytes, Oxygen consumption
|editor=[[Plangger M]]
|editor=[[Plangger M]]
}}
}}
{{Labeling}}
== Affiliations and support ==
== Affiliations and support ==
::::Marilena Karavyraki(1), Erich Gnaiger(2), Richard K. Porter(1)
:::: Marilena Karavyraki<sup>1</sup>, Erich Gnaiger<sup>2</sup>, Richard K Porter<sup>1</sup>
::::#School of Biochemistry, Trinity Biomedical Science Institute, Trinity College Dublin, Ireland.
::::# School of Biochemistry, Trinity Biomedical Science Institute, Trinity College Dublin, Ireland - rkporter@tcd.ie
::::#Oroboros Instruments, Innsbruck, Austria
::::# Oroboros Instruments, Innsbruck, Austria


::::Acknowledgements: Marie Curie Grant TRACT 721906 H2020-MCSA-ITN 2016; COST Action CA15203 (2016-2021): MitoEAGLE.
::::Acknowledgements: Marie Curie Grant TRACT 721906 H2020-MCSA-ITN 2016; COST Action CA15203 [[MitoEAGLE]] (2016-2021).
Β 
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Revision as of 08:37, 27 May 2022

Bioblast2022 banner.jpg

Porter Richard K
Karavyraki M, Gnaiger E, Porter Richard K (2022) A comparison of bioenergetics in human tongue pre-cancerous dysplastic oral keratinocytes and squamous cancer cells. Bioblast 2022: BEC Inaugural Conference.

Link: Bioblast 2022: BEC Inaugural Conference

Karavyraki Marilena, Gnaiger Erich, Porter Richard K (2022)

Event: Bioblast 2022

In an endeavour to understand the metabolic phenotype behind metastasis from 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 density but lower mitochondrial O2 flow per cell JO2 than DOK cells. The lower cell JO2 in SCC-4 cells can be partially explained by lower NADH-related enzymatic 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€’ Keywords: Oral Squamous Cancer Cells, Mitochondria, Interleukin 6, Dysplastic oral keratinocytes, Oxygen consumption β€’ Bioblast editor: Plangger M


Affiliations and support

Marilena Karavyraki1, Erich Gnaiger2, Richard K Porter1
  1. School of Biochemistry, Trinity Biomedical Science Institute, Trinity College Dublin, Ireland - [email protected]
  2. Oroboros Instruments, Innsbruck, Austria
Acknowledgements: Marie Curie Grant TRACT 721906 H2020-MCSA-ITN 2016; COST Action CA15203 MitoEAGLE (2016-2021).


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