<div class="csl-bib-body">
<div class="csl-entry">Tomin, T., Honeder, S. E., Liesinger, L., Gremel, D., Retzl, B., Lindenmann, J., Brcic, L., Schittmayer-Schantl, M., & Birner-Grünberger, R. (2024, July 3). <i>SNAPSHOT OF REDOX SIGNALING IN LUNG CANCER SUGGESTS OXIDATIVE METABOLISM PREFERENCE AND IMPAIRED GLYOXALASE SYSTEM AMID ELEVATED OXIDATIVE STRESS</i> [Poster Presentation]. ISCAM 2024, Brussels, Belgium. http://hdl.handle.net/20.500.12708/208258</div>
</div>
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dc.identifier.uri
http://hdl.handle.net/20.500.12708/208258
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dc.description.abstract
Oxidative stress is a critical driver of lung cancer progression, causing DNA and protein instability and supporting oncogenic transformation. At the metabolic level, reactive oxygen species (ROS) can oxidatively modify metabolic enzymes and reroute metabolic pathways according to tumor needs. Here, particularly important are thiol groups which act as main carriers of redox signaling, but due to their highly reactive nature are rarely analyzed in the clinical setting.
To accurately address the cross talk between redox signaling and metabolism in lung cancer, we collected tumor as well as neighboring (not directly tumor-adjacent) healthy tissue from 70 individuals with non-small cell lung cancer. We took special precautions: samples were collected at the point of surgical tumor removal and preserved immediately in a thiol-quenching solution, before being subjected to multi-omics analysis.
As a result of such unbiased redox approach we report evidence for the first time of higher oxidation of a number of key metabolic enzymes in tumor tissue, especially those involved in glucose metabolism, including phosphofructokinase (PFK), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), phosphoglycerate kinase (PGK) and pyruvate kinase M (PKM). We furthermore demonstrate indications of active efforts by the tumor to maintain oxidative metabolism amid the prominent rise of intracellular oxidative stress. Lastly, we report both redox and protein level deactivation of glyoxalase system. This might result in higher excretion of toxic methylglyoxal, potentially supporting cancer progression.
en
dc.description.sponsorship
FWF - Österr. Wissenschaftsfonds
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dc.language.iso
en
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dc.subject
lung cancer
en
dc.subject
redox stress
en
dc.subject
redox proteomics
en
dc.title
SNAPSHOT OF REDOX SIGNALING IN LUNG CANCER SUGGESTS OXIDATIVE METABOLISM PREFERENCE AND IMPAIRED GLYOXALASE SYSTEM AMID ELEVATED OXIDATIVE STRESS
en
dc.type
Presentation
en
dc.type
Vortrag
de
dc.contributor.affiliation
Medical University of Graz, Austria
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dc.relation.grantno
F 7309-B21
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dc.type.category
Poster Presentation
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tuw.project.title
Lipidhydrolyse im Krebs und in Lipid-assoziierten Krankheiten
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tuw.researchinfrastructure
Cell Culture Core Facility (CCCF)
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tuw.researchTopic.id
M6
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tuw.researchTopic.name
Biological and Bioactive Materials
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tuw.researchTopic.value
100
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tuw.publication.orgunit
E164-01-3 - Forschungsgruppe Bioanalytik
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tuw.author.orcid
0000-0002-7071-2316
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tuw.author.orcid
0000-0003-1276-7666
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tuw.author.orcid
0000-0002-9098-8416
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tuw.author.orcid
0000-0003-3249-655X
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tuw.author.orcid
0000-0003-3950-0312
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tuw.event.name
ISCAM 2024
en
tuw.event.startdate
03-07-2024
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tuw.event.enddate
05-07-2024
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tuw.event.online
On Site
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tuw.event.type
Event for scientific audience
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tuw.event.place
Brussels
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tuw.event.country
BE
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tuw.event.institution
International Society for Cancer Metabolism
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tuw.event.presenter
Tomin, Tamara
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wb.sciencebranch
Chemie
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wb.sciencebranch
Biologie
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wb.sciencebranch
Anatomie, Pathologie, Physiologie
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wb.sciencebranch.oefos
1040
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wb.sciencebranch.oefos
1060
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wb.sciencebranch.oefos
3011
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wb.sciencebranch.value
50
-
wb.sciencebranch.value
20
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wb.sciencebranch.value
30
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item.openairetype
conference poster not in proceedings
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item.cerifentitytype
Publications
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item.grantfulltext
none
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item.languageiso639-1
en
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item.openairecristype
http://purl.org/coar/resource_type/c_18co
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item.fulltext
no Fulltext
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crisitem.project.funder
FWF - Österr. Wissenschaftsfonds
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crisitem.project.grantno
F 7309-B21
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crisitem.author.dept
E164-01-3 - Forschungsgruppe Bioanalytik
-
crisitem.author.dept
E164-01-3 - Forschungsgruppe Bioanalytik
-
crisitem.author.dept
E164-01-3 - Forschungsgruppe Bioanalytik
-
crisitem.author.dept
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
-
crisitem.author.dept
E164-01-3 - Forschungsgruppe Bioanalytik
-
crisitem.author.dept
Medical University of Graz
-
crisitem.author.dept
Medical University of Graz
-
crisitem.author.dept
E164-01-3 - Forschungsgruppe Bioanalytik
-
crisitem.author.dept
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
-
crisitem.author.orcid
0000-0002-7071-2316
-
crisitem.author.orcid
0000-0003-1276-7666
-
crisitem.author.orcid
0000-0002-9098-8416
-
crisitem.author.orcid
0000-0003-3249-655X
-
crisitem.author.orcid
0000-0003-3950-0312
-
crisitem.author.parentorg
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
-
crisitem.author.parentorg
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
-
crisitem.author.parentorg
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
-
crisitem.author.parentorg
E164 - Institut für Chemische Technologien und Analytik
-
crisitem.author.parentorg
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
-
crisitem.author.parentorg
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
-
crisitem.author.parentorg
E164 - Institut für Chemische Technologien und Analytik
