<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. (2025, June 12). <i>Increased antioxidative defense and reduced advanced glycation end product formation by metabolic adaptation in Non-Small-Cell-Lung-Cancer patients</i> [Poster Presentation]. CCC-TRI Symposium, Vienna, Austria.</div>
</div>
Background
Cancer cells use multiple mechanisms to counteract oxidative stress. Reactive oxygen species can oxidatively modify enzymes to reroute metabolic pathways according to tumor needs, e.g., for antioxidant production/recycling. Therefore, identification of oxidized proteins is an important step for understanding mechanisms that drive cancer cell survival. Thiol groups are most susceptible to oxidative modifications but rarely analyzed in clinical settings due to their reactivity and associated post-sampling artifacts.
Methods
To accurately address the cross-talk between redox signaling and metabolism we collected tumor and healthy tissue from 70 individuals with non-small cell lung cancer right after surgery into a thiol-quenching solution, then carried out redox-proteomics and small molecular thiol analysis.
Results and conclusions
As a result of such an unbiased approach, we for the first-time show evidence of higher oxidation of a number of proteins linked to pro-oncogenic pathways including key metabolic enzymes in human tumors (especially glucose-related). We demonstrate that cancer adapts metabolism to increase glutathione synthesis to fight the rise of intracellular oxidative stress. Glyoxalases, the key enzymes in the detoxification of methylglyoxal, a byproduct of glycolysis and precursor of advanced glycation end products, were compromised by oxidative modifications and downregulation on protein level. Despite decreased methylglyoxal detoxification capacity, however, cancers did not accumulate advanced glycation end products. Since downregulation or inhibition of GAPDH activity led to upregulation of glyoxalases in non-small cell lung cancer cells we propose that tumors efficiently avoid methylglyoxal formation by upregulation of GAPDH activity.
en
dc.description.sponsorship
FWF - Österr. Wissenschaftsfonds
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dc.language.iso
en
-
dc.subject
redox-proteomics
en
dc.title
Increased antioxidative defense and reduced advanced glycation end product formation by metabolic adaptation in Non-Small-Cell-Lung-Cancer patients
en
dc.type
Presentation
en
dc.type
Vortrag
de
dc.contributor.affiliation
TU Wien, Austria
-
dc.contributor.affiliation
TU Wien, Austria
-
dc.contributor.affiliation
Technisches Museum Wien, Austria
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dc.contributor.affiliation
Medical University of Vienna, Austria
-
dc.relation.grantno
F 7309-B21
-
dc.type.category
Poster Presentation
-
tuw.project.title
Lipidhydrolyse im Krebs und in Lipid-assoziierten Krankheiten
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tuw.researchinfrastructure
Cell Culture Core Facility (CCCF)
-
tuw.researchTopic.id
X1
-
tuw.researchTopic.name
Beyond TUW-research focus
-
tuw.researchTopic.value
100
-
tuw.publication.orgunit
E164-01-3 - Forschungsgruppe Bioanalytik
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tuw.publication.orgunit
E056-12 - Fachbereich ENROL DP
-
tuw.author.orcid
0000-0002-7071-2316
-
tuw.author.orcid
0000-0002-7201-6293
-
tuw.author.orcid
0009-0002-8635-2375
-
tuw.author.orcid
0000-0001-7764-7046
-
tuw.author.orcid
0000-0003-1276-7666
-
tuw.author.orcid
0000-0002-9098-8416
-
tuw.author.orcid
0000-0003-3249-655X
-
tuw.author.orcid
0000-0003-3950-0312
-
tuw.event.name
CCC-TRI Symposium
en
tuw.event.startdate
12-06-2025
-
tuw.event.enddate
13-06-2025
-
tuw.event.online
On Site
-
tuw.event.type
Event for scientific audience
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tuw.event.place
Vienna
-
tuw.event.country
AT
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tuw.event.presenter
Tomin, Tamara
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wb.sciencebranch
Chemie
-
wb.sciencebranch
Biologie
-
wb.sciencebranch
Anatomie, Pathologie, Physiologie
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wb.sciencebranch.oefos
1040
-
wb.sciencebranch.oefos
1060
-
wb.sciencebranch.oefos
3011
-
wb.sciencebranch.value
50
-
wb.sciencebranch.value
25
-
wb.sciencebranch.value
25
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item.languageiso639-1
en
-
item.openairetype
conference poster not in proceedings
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item.openairecristype
http://purl.org/coar/resource_type/c_18co
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item.grantfulltext
none
-
item.cerifentitytype
Publications
-
item.fulltext
no Fulltext
-
crisitem.author.dept
E164-01-3 - Forschungsgruppe Bioanalytik
-
crisitem.author.dept
TU Wien, Austria
-
crisitem.author.dept
TU Wien, Austria
-
crisitem.author.dept
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
-
crisitem.author.dept
Technisches Museum Wien, Austria
-
crisitem.author.dept
Medical University of Vienna, Austria
-
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
0000-0002-7201-6293
-
crisitem.author.orcid
0009-0002-8635-2375
-
crisitem.author.orcid
0000-0001-7764-7046
-
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 - Institut für Chemische Technologien und Analytik
-
crisitem.author.parentorg
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
-
crisitem.author.parentorg
E164 - Institut für Chemische Technologien und Analytik