Next Article in Journal
Polysaccharide-Based Systems for Targeted Stem Cell Differentiation and Bone Regeneration
Next Article in Special Issue
Metformin: The Answer to Cancer in a Flower? Current Knowledge and Future Prospects of Metformin as an Anti-Cancer Agent in Breast Cancer
Previous Article in Journal / Special Issue
Honokiol Enhances TRAIL-Mediated Apoptosis through STAMBPL1-Induced Survivin and c-FLIP Degradation
Open AccessArticle

Benzyl Isothiocyanate Induces Apoptosis via Reactive Oxygen Species-Initiated Mitochondrial Dysfunction and DR4 and DR5 Death Receptor Activation in Gastric Adenocarcinoma Cells

1
Cell Signaling and Pharmacological Activity Lab, Department of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Korea
2
Neuropharmacology and Stem Cell Lab, Department of Pharmacology, College of Pharmacy, Chung-Ang University, Seoul 06974, Korea
*
Authors to whom correspondence should be addressed.
Biomolecules 2019, 9(12), 839; https://doi.org/10.3390/biom9120839
Received: 22 October 2019 / Revised: 26 November 2019 / Accepted: 1 December 2019 / Published: 6 December 2019
Benzyl isothiocyanate (BITC) is known to inhibit the metastasis of gastric cancer cells but further studies are needed to confirm its chemotherapeutic potential against gastric cancer. In this study, we observed cell shrinkage and morphological changes in one of the gastric adenocarcinoma cell lines, the AGS cells, after BITC treatment. We performed 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay, a cell viability assay, and found that BITC decreased AGS cell viability. Reactive oxygen species (ROS) analyses using 2′,7′-dichlorofluorescin diacetate (DCFDA) revealed that BITC-induced cell death involved intracellular ROS production, which resulted in mitochondrial dysfunction. Additionally, cell viability was partially restored when BITC-treated AGS cells were preincubated with glutathione (GSH). Western blotting indicated that BITC regulated the expressions of the mitochondria-mediated apoptosis signaling molecules, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), and cytochrome c (Cyt c). In addition, BITC increased death receptor DR5 expression, and activated the cysteine-aspartic proteases (caspases) cascade. Overall, our results showed that BITC triggers apoptosis in AGS cells via the apoptotic pathways involved in ROS-promoted mitochondrial dysfunction and death receptor activation. View Full-Text
Keywords: benzyl isothiocyanate; gastric cancer; apoptosis; reactive oxygen species; death receptors; natural product benzyl isothiocyanate; gastric cancer; apoptosis; reactive oxygen species; death receptors; natural product
Show Figures

Figure 1

MDPI and ACS Style

Han, K.W.W.; Po, W.W.; Sohn, U.D.; Kim, H.-J. Benzyl Isothiocyanate Induces Apoptosis via Reactive Oxygen Species-Initiated Mitochondrial Dysfunction and DR4 and DR5 Death Receptor Activation in Gastric Adenocarcinoma Cells. Biomolecules 2019, 9, 839.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop