<div class="csl-bib-body">
<div class="csl-entry">Lachmann, J., Honeder, S. E., Hofreither, D., Liesinger, L., Schittmayer-Schantl, M., Tomin, T., & Birner-Grünberger, R. (2026). <i>Role of neutral lipolysis in cellular signaling in lung cancer</i> [Poster Presentation]. 10th International Graz Symposium on Lipid and Membrane Biology, Graz, Austria.</div>
</div>
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dc.identifier.uri
http://hdl.handle.net/20.500.12708/229655
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dc.description.abstract
Lipid metabolism plays an essential role in lung physiology—pulmonary environment is rich in specific lipid classes and enzymes involved in lipid synthesis, remodeling and degradation. Disruptions of lipid metabolism have been implicated in the pathogenesis of lung cancer, making the understanding of lipid signaling critical for the elucidation of underlying disease mechanisms and identification of potential therapeutic targets.
It remains poorly understood how altered expression of different lipid hydrolases shape signaling, redox balancing and cellular responses such as proliferation or apoptosis of lung cancer cells. In this study, we investigated the impact of overexpression and knockout of the two key lipid hydrolases, adipose triglyceride lipase (ATGL) and monoacylglycerol lipase (MGL), on lipid signaling in lung cancer cell lines under nutrient-replete and lipid starved conditions. That was achieved by performing small-molecular thiols analyses and phospho-proteomics to map oxidative stress and the underlying signaling pathways. Lipase-dependent regulation of apoptosis was assessed using Annexin V assays.
As a result, we report that stimulation of lipid hydrolysis causes cellular apoptosis under nutrient-replete as well as lipid starved condition and alters cellular redox status. Total glutathione levels, normalized to protein content, were reduced in lipase-overexpressing cells compared to controls under nutrient-replete conditions. Furthermore, lipid starvation decreased the ratio of reduced to oxidized glutathione relative to nutrient-replete conditions. In addition, we provide a comprehensive insight into phospho-proteome adaptation under differential expression of neutral lipases.
en
dc.description.sponsorship
FWF - Österr. Wissenschaftsfonds
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dc.language.iso
en
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dc.subject
signaling
en
dc.subject
phosphoproteomics
en
dc.subject
lipase
en
dc.subject
lung cancer
en
dc.title
Role of neutral lipolysis in cellular signaling in lung cancer
en
dc.type
Presentation
en
dc.type
Vortrag
de
dc.contributor.affiliation
TU Wien, 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
X1
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tuw.researchTopic.name
Beyond TUW-research focus
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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.publication.orgunit
E056-12 - Fachbereich ENROL DP
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tuw.author.orcid
0000-0003-3249-655X
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tuw.author.orcid
0000-0002-7071-2316
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tuw.author.orcid
0000-0003-3950-0312
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tuw.event.name
10th International Graz Symposium on Lipid and Membrane Biology
en
tuw.event.startdate
16-04-2026
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tuw.event.enddate
18-04-2026
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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
Graz
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tuw.event.country
AT
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tuw.event.presenter
Lachmann, Johanna
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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
30
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wb.sciencebranch.value
20
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item.fulltext
no Fulltext
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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.cerifentitytype
Publications
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item.grantfulltext
none
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item.openairetype
conference poster not in proceedings
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crisitem.author.dept
TU Wien, Austria
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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
E164-01-3 - Forschungsgruppe Bioanalytik
-
crisitem.author.dept
E164-01-3 - Forschungsgruppe Bioanalytik
-
crisitem.author.dept
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
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crisitem.author.orcid
0000-0003-3249-655X
-
crisitem.author.orcid
0000-0002-7071-2316
-
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
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
-
crisitem.author.parentorg
E164-01 - Forschungsbereich Imaging und Instrumentelle Analytische Chemie
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crisitem.author.parentorg
E164 - Institut für Chemische Technologien und Analytik
