Vorinostat Treatment of Gastric Cancer Cells Leads to ROS-Induced Cell Inhibition and a Complex Pattern of Molecular Alterations in Nrf2-Dependent Genes Article Swipe
Leoni Lorenz
,
Tamara Zenz
,
Denys Oliinyk
,
Florian Meier-Rosar
,
Robert Jenke
,
Achim Aigner
,
Thomas Büch
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.3390/ph17081080
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.3390/ph17081080
Histone deacetylase inhibitors (HDACi) show high antineoplastic potential in preclinical studies in various solid tumors, including gastric carcinoma; however, their use in clinical studies has not yet yielded convincing efficacies. Thus, further studies on cellular/molecular effects of HDACi are needed, for improving clinical efficacy and identifying suitable combination partners. Here, we investigated the role of oxidative stress in gastric cancer cells upon treatment with HDACi. A particular focus was laid on the role of the Nrf2 pathway, which can mediate resistance to cell-inhibitory effects of reactive oxidative species (ROS). Using fluorescence-based ROS sensors, oxidative stress was measured in human gastric cancer cell lines. Activation of the Nrf2 pathway was monitored in luciferase reporter assays as well as by mRNA and proteomic expression analyses of Nrf2 regulators and Nrf2-induced genes. Furthermore, the effects of ROS scavenger N-acetyl-L-cysteine (NAC) and Nrf2-knockdown on HDACi-dependent antiproliferative effects were investigated in colorimetric formazan-based and clonogenic survival assays. HDACi treatment led to increased oxidative stress levels and consequently, treatment with NAC reduced cytotoxicity of HDACi. In addition, vorinostat treatment stimulated expression of a luciferase reporter under the control of an antioxidative response element, indicating activation of the Nrf2 system. This Nrf2 activation was only partially reversible by treatment with NAC, suggesting ROS independent pathways to contribute to HDACi-promoted Nrf2 activation. In line with its cytoprotective role, Nrf2 knockdown led to a sensitization against HDACi. Accordingly, the expression of antioxidant and detoxifying Nrf2 target genes was upregulated upon HDACi treatment. In conclusion, oxidative stress induction upon HDAC inhibition contributes to the antitumor effects of HDAC inhibitors, and activation of Nrf2 represents a potentially important adaptive response of gastric cancer cells in this context.
Related Topics
Concepts
Vorinostat
Gene knockdown
Oxidative stress
Cancer research
Histone deacetylase
Reactive oxygen species
Chemistry
Histone deacetylase inhibitor
Luciferase
Downregulation and upregulation
Clonogenic assay
Pharmacology
Biology
Transfection
Cell
Histone
Biochemistry
Apoptosis
Gene
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.3390/ph17081080
- https://www.mdpi.com/1424-8247/17/8/1080/pdf?version=1724039483
- OA Status
- gold
- Cited By
- 2
- References
- 54
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4401634998
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4401634998Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.3390/ph17081080Digital Object Identifier
- Title
-
Vorinostat Treatment of Gastric Cancer Cells Leads to ROS-Induced Cell Inhibition and a Complex Pattern of Molecular Alterations in Nrf2-Dependent GenesWork title
- Type
-
articleOpenAlex work type
- Language
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enPrimary language
- Publication year
-
2024Year of publication
- Publication date
-
2024-08-16Full publication date if available
- Authors
-
Leoni Lorenz, Tamara Zenz, Denys Oliinyk, Florian Meier-Rosar, Robert Jenke, Achim Aigner, Thomas BüchList of authors in order
- Landing page
-
https://doi.org/10.3390/ph17081080Publisher landing page
- PDF URL
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https://www.mdpi.com/1424-8247/17/8/1080/pdf?version=1724039483Direct link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
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https://www.mdpi.com/1424-8247/17/8/1080/pdf?version=1724039483Direct OA link when available
- Concepts
-
Vorinostat, Gene knockdown, Oxidative stress, Cancer research, Histone deacetylase, Reactive oxygen species, Chemistry, Histone deacetylase inhibitor, Luciferase, Downregulation and upregulation, Clonogenic assay, Pharmacology, Biology, Transfection, Cell, Histone, Biochemistry, Apoptosis, GeneTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
2Total citation count in OpenAlex
- Citations by year (recent)
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2025: 2Per-year citation counts (last 5 years)
- References (count)
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54Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.induction | 247 |
| abstract_inverted_index.knockdown | 221 |
| abstract_inverted_index.monitored | 109 |
| abstract_inverted_index.oxidative | 55, 86, 93, 157, 245 |
| abstract_inverted_index.partially | 198 |
| abstract_inverted_index.partners. | 48 |
| abstract_inverted_index.potential | 7 |
| abstract_inverted_index.proteomic | 120 |
| abstract_inverted_index.scavenger | 134 |
| abstract_inverted_index.treatment | 62, 153, 162, 172, 201 |
| abstract_inverted_index.Activation | 103 |
| abstract_inverted_index.activation | 188, 195, 260 |
| abstract_inverted_index.carcinoma; | 17 |
| abstract_inverted_index.clonogenic | 149 |
| abstract_inverted_index.contribute | 209 |
| abstract_inverted_index.convincing | 28 |
| abstract_inverted_index.expression | 121, 174, 230 |
| abstract_inverted_index.indicating | 187 |
| abstract_inverted_index.inhibition | 250 |
| abstract_inverted_index.inhibitors | 2 |
| abstract_inverted_index.luciferase | 111, 177 |
| abstract_inverted_index.particular | 66 |
| abstract_inverted_index.regulators | 125 |
| abstract_inverted_index.represents | 263 |
| abstract_inverted_index.resistance | 80 |
| abstract_inverted_index.reversible | 199 |
| abstract_inverted_index.stimulated | 173 |
| abstract_inverted_index.suggesting | 204 |
| abstract_inverted_index.treatment. | 242 |
| abstract_inverted_index.vorinostat | 171 |
| abstract_inverted_index.activation. | 213 |
| abstract_inverted_index.antioxidant | 232 |
| abstract_inverted_index.combination | 47 |
| abstract_inverted_index.conclusion, | 244 |
| abstract_inverted_index.contributes | 251 |
| abstract_inverted_index.deacetylase | 1 |
| abstract_inverted_index.detoxifying | 234 |
| abstract_inverted_index.efficacies. | 29 |
| abstract_inverted_index.identifying | 45 |
| abstract_inverted_index.independent | 206 |
| abstract_inverted_index.inhibitors, | 258 |
| abstract_inverted_index.potentially | 265 |
| abstract_inverted_index.preclinical | 9 |
| abstract_inverted_index.upregulated | 239 |
| abstract_inverted_index.Accordingly, | 228 |
| abstract_inverted_index.Furthermore, | 129 |
| abstract_inverted_index.Nrf2-induced | 127 |
| abstract_inverted_index.colorimetric | 146 |
| abstract_inverted_index.cytotoxicity | 166 |
| abstract_inverted_index.investigated | 51, 144 |
| abstract_inverted_index.antioxidative | 184 |
| abstract_inverted_index.consequently, | 161 |
| abstract_inverted_index.sensitization | 225 |
| abstract_inverted_index.HDACi-promoted | 211 |
| abstract_inverted_index.Nrf2-knockdown | 138 |
| abstract_inverted_index.antineoplastic | 6 |
| abstract_inverted_index.cytoprotective | 218 |
| abstract_inverted_index.formazan-based | 147 |
| abstract_inverted_index.HDACi-dependent | 140 |
| abstract_inverted_index.cell-inhibitory | 82 |
| abstract_inverted_index.antiproliferative | 141 |
| abstract_inverted_index.cellular/molecular | 34 |
| abstract_inverted_index.fluorescence-based | 90 |
| abstract_inverted_index.N-acetyl-L-cysteine | 135 |
| cited_by_percentile_year.max | 97 |
| cited_by_percentile_year.min | 95 |
| corresponding_author_ids | https://openalex.org/A5066560034, https://openalex.org/A5077066668 |
| countries_distinct_count | 1 |
| institutions_distinct_count | 7 |
| corresponding_institution_ids | https://openalex.org/I4210100919, https://openalex.org/I926574661 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.6200000047683716 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.69485414 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |