Data from γ-Tocotrienol Promotes TRAIL-Induced Apoptosis through Reactive Oxygen Species/Extracellular Signal-Regulated Kinase/p53–Mediated Upregulation of Death Receptors Article Swipe
Ramaswamy Kannappan
,
Jayaraj Ravindran
,
Sahdeo Prasad
,
Bokyung Sung
,
Vivek R. Yadav
,
Simone Reuter
,
Madan M. Chaturvedi
,
Bharat B. Aggarwal
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/1535-7163.c.6531644.v1
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/1535-7163.c.6531644.v1
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a member of the tumor necrosis factor superfamily, is in clinical trials for cancer therapy, but its anticancer potential is limited by the development of resistance. We investigated the ability of tocotrienol (T3), an unsaturated vitamin E present in palm oil, rice bran, barley, oats, and wheat germ, to sensitize tumor cells to TRAIL. Results from esterase staining, colony formation, caspase activation, and sub-G1 cell cycle arrest revealed that γ-T3 can sensitize human colon cancer cells to TRAIL. When examined for the mechanism, we found that γ-T3 significantly downregulated the expression of antiapoptotic proteins (c-IAP2 and Bcl-xL). We also found that γ-T3, but not tocopherol, induced the expression of the TRAIL receptors death receptor (DR)-4 and DR5. This induction was not cell type specific, as upregulation was also found in pancreatic, kidney, and leukemic cells. Upregulation of DRs by γ-T3 required the production of reactive oxygen species (ROS), and sequestering of ROS abolished both upregulation of the receptors and potentiation of TRAIL-induced apoptosis. Induction of DRs by γ-T3 also required activation of extracellular signal-regulated kinase 1 (ERK1), as silencing of ERK1 by specific siRNA abrogated the upregulation of TRAIL receptors. Further, induction of DRs by γ-T3 required the expression of p53 and Bax, as no induction of the receptors was found in colon cancer cells with deletion of these genes. Overall, our results show that γ-T3 sensitizes tumor cells to TRAIL by upregulating DRs through the ROS/ERK/p53 pathway and by downregulating cell survival proteins. Mol Cancer Ther; 9(8); 2196–207. ©2010 AACR.
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Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1158/1535-7163.c.6531644.v1
- OA Status
- gold
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4361958416
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4361958416Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1158/1535-7163.c.6531644.v1Digital Object Identifier
- Title
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Data from γ-Tocotrienol Promotes TRAIL-Induced Apoptosis through Reactive Oxygen Species/Extracellular Signal-Regulated Kinase/p53–Mediated Upregulation of Death ReceptorsWork title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2023Year of publication
- Publication date
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2023-03-31Full publication date if available
- Authors
-
Ramaswamy Kannappan, Jayaraj Ravindran, Sahdeo Prasad, Bokyung Sung, Vivek R. Yadav, Simone Reuter, Madan M. Chaturvedi, Bharat B. AggarwalList of authors in order
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https://doi.org/10.1158/1535-7163.c.6531644.v1Publisher landing page
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YesWhether a free full text is available
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goldOpen access status per OpenAlex
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https://doi.org/10.1158/1535-7163.c.6531644.v1Direct OA link when available
- Concepts
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Downregulation and upregulation, Tumor necrosis factor alpha, Reactive oxygen species, Receptor, Apoptosis, Biology, Cancer research, Signal transduction, Programmed cell death, Cell biology, Molecular biology, Chemistry, Immunology, Biochemistry, GeneTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.receptors | 117, 163, 214 |
| abstract_inverted_index.sensitize | 55, 77 |
| abstract_inverted_index.silencing | 184 |
| abstract_inverted_index.specific, | 129 |
| abstract_inverted_index.staining, | 63 |
| abstract_inverted_index.activation | 176 |
| abstract_inverted_index.anticancer | 23 |
| abstract_inverted_index.apoptosis. | 168 |
| abstract_inverted_index.expression | 96, 113, 204 |
| abstract_inverted_index.formation, | 65 |
| abstract_inverted_index.mechanism, | 88 |
| abstract_inverted_index.production | 148 |
| abstract_inverted_index.receptors. | 195 |
| abstract_inverted_index.sensitizes | 232 |
| abstract_inverted_index.2196–207. | 254 |
| abstract_inverted_index.ROS/ERK/p53 | 242 |
| abstract_inverted_index.activation, | 67 |
| abstract_inverted_index.development | 29 |
| abstract_inverted_index.pancreatic, | 136 |
| abstract_inverted_index.resistance. | 31 |
| abstract_inverted_index.tocopherol, | 110 |
| abstract_inverted_index.tocotrienol | 37 |
| abstract_inverted_index.unsaturated | 40 |
| abstract_inverted_index.Upregulation | 141 |
| abstract_inverted_index.investigated | 33 |
| abstract_inverted_index.potentiation | 165 |
| abstract_inverted_index.sequestering | 155 |
| abstract_inverted_index.superfamily, | 13 |
| abstract_inverted_index.upregulating | 238 |
| abstract_inverted_index.upregulation | 131, 160, 192 |
| abstract_inverted_index.TRAIL-induced | 167 |
| abstract_inverted_index.antiapoptotic | 98 |
| abstract_inverted_index.downregulated | 94 |
| abstract_inverted_index.extracellular | 178 |
| abstract_inverted_index.significantly | 93 |
| abstract_inverted_index.downregulating | 246 |
| abstract_inverted_index.factor-related | 2 |
| abstract_inverted_index.signal-regulated | 179 |
| abstract_inverted_index.apoptosis-inducing | 3 |
| abstract_inverted_index.AACR.</p></div> | 256 |
| abstract_inverted_index.sub-G<sub>1</sub> | 69 |
| abstract_inverted_index.<div>Abstract<p>Tumor | 0 |
| cited_by_percentile_year | |
| countries_distinct_count | 0 |
| institutions_distinct_count | 8 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.550000011920929 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.12682925 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |