Potential effects of allyl isothiocyanate on inhibiting cellular proliferation and inducing apoptotic pathway in human cisplatin-resistant oral cancer cells
Background/purpose: Cisplatin-resistant oral cancer is clinically difficult to manage and the dose-dependent toxicities of cisplatin has been widely concerned. Allyl isothiocyanate (AITC), known as mustard oil, is a plant-derived compound abundant in cruciferous vegetables. It is reported to have an...
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| Format: | Article |
| Language: | English |
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Elsevier
2021-01-01
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| Series: | Journal of the Formosan Medical Association |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0929664620302850 |
| _version_ | 1818603728755752960 |
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| author | Pei-ying Chang Fuu-jen Tsai Da-tian Bau Yuan-man Hsu Jai-sing Yang Ming-gene Tu Shang-lun Chiang |
| author_facet | Pei-ying Chang Fuu-jen Tsai Da-tian Bau Yuan-man Hsu Jai-sing Yang Ming-gene Tu Shang-lun Chiang |
| author_sort | Pei-ying Chang |
| collection | DOAJ |
| description | Background/purpose: Cisplatin-resistant oral cancer is clinically difficult to manage and the dose-dependent toxicities of cisplatin has been widely concerned. Allyl isothiocyanate (AITC), known as mustard oil, is a plant-derived compound abundant in cruciferous vegetables. It is reported to have anti-cancer potential as a natural dietary chemopreventive compound against a variety of cancers, but the effect of AITC on cisplatin-resistant cancer cells is still little-known. Methods: Human CAL27-cisplatin-resistant oral cancer cells (CAR cells) were examined to investigate the antitumor properties of AITC. 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay, IncuCyte™ S3 cell proliferation assay, 4′,6-diamidino-2-phenylindole (DAPI) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining as well as Western blot analysis were deployed. Results: AITC decreased CAR cell viability, induced cell death of CAR cells and inhibited the confluences of cultured CAR cells. When CAR cells were treated with AITC, activation of caspase-3 and caspase-9 by AITC was observed and could be reversed by Z-VAD-fmk (pan-caspase inhibitor). Furthermore, the protein expressions of phosphorylated protein kinase B (p-AKT) and phosphorylated mammalian target of rapamycin (p-mTOR) were suppressed in AITC-treated CAR cells, whereas protein expressions of Bax, cytochrome c, Apaf-1, cleaved caspase-3, and cleaved caspase-9 were upregulated in AITC-treated CAR cells. Conclusion: AITC can inhibit Akt/mTOR proliferation signaling and promote mitochondria-dependent apoptotic pathway through AITC-enhanced activities of caspase-3 and caspase-9 in CAR cells. |
| first_indexed | 2024-12-16T13:27:47Z |
| format | Article |
| id | doaj.art-fa1e4bb3abac48d7bb84a2e82ba09391 |
| institution | Directory Open Access Journal |
| issn | 0929-6646 |
| language | English |
| last_indexed | 2024-12-16T13:27:47Z |
| publishDate | 2021-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of the Formosan Medical Association |
| spelling | doaj.art-fa1e4bb3abac48d7bb84a2e82ba093912022-12-21T22:30:11ZengElsevierJournal of the Formosan Medical Association0929-66462021-01-011201515523Potential effects of allyl isothiocyanate on inhibiting cellular proliferation and inducing apoptotic pathway in human cisplatin-resistant oral cancer cellsPei-ying Chang0Fuu-jen Tsai1Da-tian Bau2Yuan-man Hsu3Jai-sing Yang4Ming-gene Tu5Shang-lun Chiang6Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan; School of Dentistry, China Medical University, Taichung, TaiwanSchool of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan; China Medical University Children's Hospital, China Medical University, Taichung, TaiwanGraduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan; Terry Fox Cancer Research Laboratory, Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, Taiwan; Department of Bioinformatics and Medical Engineering, Asia University, Taichung, TaiwanDepartment of Biological Science and Technology, China Medical University, Taichung, TaiwanDepartment of Medical Research, China Medical University Hospital, China Medical University, Taichung, TaiwanSchool of Dentistry, China Medical University, Taichung, Taiwan; Department of Dentistry, China Medical University Hospital, Taichung, Taiwan; Corresponding author. School of Dentistry, China Medical University, No 91, Hsueh-Shih Road, Taichung, Taiwan,Environment-Omics-Disease Research Center, China Medical University Hospital, Taichung, Taiwan; Department of Public Health, College of Public Health, China Medical University, Taichung, Taiwan; Corresponding author. Shang-lun Chiang, Department of Public Health, College of Public Health, China Medical University, No 91, Hsueh-Shih Road, Taichung. Taiwan.Background/purpose: Cisplatin-resistant oral cancer is clinically difficult to manage and the dose-dependent toxicities of cisplatin has been widely concerned. Allyl isothiocyanate (AITC), known as mustard oil, is a plant-derived compound abundant in cruciferous vegetables. It is reported to have anti-cancer potential as a natural dietary chemopreventive compound against a variety of cancers, but the effect of AITC on cisplatin-resistant cancer cells is still little-known. Methods: Human CAL27-cisplatin-resistant oral cancer cells (CAR cells) were examined to investigate the antitumor properties of AITC. 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay, IncuCyte™ S3 cell proliferation assay, 4′,6-diamidino-2-phenylindole (DAPI) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining as well as Western blot analysis were deployed. Results: AITC decreased CAR cell viability, induced cell death of CAR cells and inhibited the confluences of cultured CAR cells. When CAR cells were treated with AITC, activation of caspase-3 and caspase-9 by AITC was observed and could be reversed by Z-VAD-fmk (pan-caspase inhibitor). Furthermore, the protein expressions of phosphorylated protein kinase B (p-AKT) and phosphorylated mammalian target of rapamycin (p-mTOR) were suppressed in AITC-treated CAR cells, whereas protein expressions of Bax, cytochrome c, Apaf-1, cleaved caspase-3, and cleaved caspase-9 were upregulated in AITC-treated CAR cells. Conclusion: AITC can inhibit Akt/mTOR proliferation signaling and promote mitochondria-dependent apoptotic pathway through AITC-enhanced activities of caspase-3 and caspase-9 in CAR cells.http://www.sciencedirect.com/science/article/pii/S0929664620302850AITCApoptosisCAR cellsCisplatin resistanceOSCC |
| spellingShingle | Pei-ying Chang Fuu-jen Tsai Da-tian Bau Yuan-man Hsu Jai-sing Yang Ming-gene Tu Shang-lun Chiang Potential effects of allyl isothiocyanate on inhibiting cellular proliferation and inducing apoptotic pathway in human cisplatin-resistant oral cancer cells Journal of the Formosan Medical Association AITC Apoptosis CAR cells Cisplatin resistance OSCC |
| title | Potential effects of allyl isothiocyanate on inhibiting cellular proliferation and inducing apoptotic pathway in human cisplatin-resistant oral cancer cells |
| title_full | Potential effects of allyl isothiocyanate on inhibiting cellular proliferation and inducing apoptotic pathway in human cisplatin-resistant oral cancer cells |
| title_fullStr | Potential effects of allyl isothiocyanate on inhibiting cellular proliferation and inducing apoptotic pathway in human cisplatin-resistant oral cancer cells |
| title_full_unstemmed | Potential effects of allyl isothiocyanate on inhibiting cellular proliferation and inducing apoptotic pathway in human cisplatin-resistant oral cancer cells |
| title_short | Potential effects of allyl isothiocyanate on inhibiting cellular proliferation and inducing apoptotic pathway in human cisplatin-resistant oral cancer cells |
| title_sort | potential effects of allyl isothiocyanate on inhibiting cellular proliferation and inducing apoptotic pathway in human cisplatin resistant oral cancer cells |
| topic | AITC Apoptosis CAR cells Cisplatin resistance OSCC |
| url | http://www.sciencedirect.com/science/article/pii/S0929664620302850 |
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