Version 1
: Received: 25 July 2024 / Approved: 25 July 2024 / Online: 26 July 2024 (04:27:29 CEST)
How to cite:
Kim, H. H.; Lee, D.-H. Apoptosis of Pancreatic Cancer Cells after Co-treatment with Eugenol and Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand. Preprints2024, 2024072074. https://doi.org/10.20944/preprints202407.2074.v1
Kim, H. H.; Lee, D.-H. Apoptosis of Pancreatic Cancer Cells after Co-treatment with Eugenol and Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand. Preprints 2024, 2024072074. https://doi.org/10.20944/preprints202407.2074.v1
Kim, H. H.; Lee, D.-H. Apoptosis of Pancreatic Cancer Cells after Co-treatment with Eugenol and Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand. Preprints2024, 2024072074. https://doi.org/10.20944/preprints202407.2074.v1
APA Style
Kim, H. H., & Lee, D. H. (2024). Apoptosis of Pancreatic Cancer Cells after Co-treatment with Eugenol and Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand. Preprints. https://doi.org/10.20944/preprints202407.2074.v1
Chicago/Turabian Style
Kim, H. H. and Dae-Hee Lee. 2024 "Apoptosis of Pancreatic Cancer Cells after Co-treatment with Eugenol and Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand" Preprints. https://doi.org/10.20944/preprints202407.2074.v1
Abstract
Pancreatic cancer is a refractory cancer with limited treatment options. Various cancer types are resistant to the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Eugenol, the main component of clove oil, exhibits anticancer, anti-inflammatory, and antioxidant effects. However, no studies have reported that eugenol increases TRAIL sensitivity by upregulating death receptor (DR) expression. Here, we aimed to investigate eugenol as a potent TRAIL sensitizer. Increased apoptosis and inhibition of cell proliferation was observed in pancreatic cancer cells treated with eugenol and TRAIL compared with those treated with eugenol alone. Eugenol upregulated the expression of DR5, inhibited FLICE-inhibitory protein (FLIP), an anti-apoptotic protein, and increased p53, a tumor suppressor protein. In addition, eugenol induced the generation of reactive oxygen species (ROS) and caused endoplasmic reticulum (ER) stress. C/EBP-homologous protein (CHOP) knockdown using siRNA decreased the expression of DR5 and reduced the combined effects of eugenol and TRAIL. These results demonstrate that eugenol enhances TRAIL-induced apoptosis by upregulating DR5 through the ROS-mediated ER stress-CHOP pathway, enhancing ER stress by inducing p53 and downregulating FLIP expression. This suggests that eugenol has the potential to treat pancreatic cancer by increasing cell sensitivity to TRAIL.
Biology and Life Sciences, Cell and Developmental Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
