Seselin promotes cisplatin-induced apoptosis of AGS gastric cancer cells by inhibiting β-catenin expression

Gastric cancer is a commonly diagnosed form of cancer, and cisplatin is commonly used as a chemotherapy drug for treating it. However, the side effects of cisplatin may reduce patients’ willingness to use it. Seselin, a derivative of coumarin, has been found to have anticancer properties as well as...

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Main Authors: Shyu Rong-Yaun, Wang Chun-Hua, Wu Chang-Chieh, Wang Lu-Kai, Tsai Fu-Ming
Format: Article
Language:English
Published: University of Belgrade, University of Novi Sad 2023-01-01
Series:Archives of Biological Sciences
Subjects:
Online Access:https://doiserbia.nb.rs/img/doi/0354-4664/2023/0354-46642300023S.pdf
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author Shyu Rong-Yaun
Wang Chun-Hua
Wu Chang-Chieh
Wang Lu-Kai
Tsai Fu-Ming
author_facet Shyu Rong-Yaun
Wang Chun-Hua
Wu Chang-Chieh
Wang Lu-Kai
Tsai Fu-Ming
author_sort Shyu Rong-Yaun
collection DOAJ
description Gastric cancer is a commonly diagnosed form of cancer, and cisplatin is commonly used as a chemotherapy drug for treating it. However, the side effects of cisplatin may reduce patients’ willingness to use it. Seselin, a derivative of coumarin, has been found to have anticancer properties as well as anticoagulant effects. In this study, we investigated the effect of seselin on promoting cisplatin-induced gastric cancer cell death using the cell proliferation reagent WST-1, BrdU incorporation and lactate dehydrogenase release. The role of seselin and cisplatin in the apoptosis of gastric cancer cells was analyzed using a phospho-kinase array and Western blot analysis. Seselin did not affect G2/M stasis, but it promoted cell death in AGS cells treated with cisplatin. Phospho-kinase array analysis revealed that cisplatin regulates intracellular p53 phosphorylation, while seselin regulates intracellular β-catenin expression by affecting the phosphorylation of glycogen synthase kinase-3 beta (GSK-3β), extracellular-signal-regulated kinase (ERK) and Src tyrosine kinase. Seselin and cisplatin promote the apoptosis of gastric cancer cells by the synergistic effect of two distinct signaling pathways. These findings suggest that seselin may be used as a complementary therapy to reduce the clinical dose of chemotherapy.
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spelling doaj.art-d78acc3f15d04c6680137cd34ddc3fba2023-12-12T13:06:47ZengUniversity of Belgrade, University of Novi SadArchives of Biological Sciences0354-46641821-43392023-01-0175328729710.2298/ABS230314023S0354-46642300023SSeselin promotes cisplatin-induced apoptosis of AGS gastric cancer cells by inhibiting β-catenin expressionShyu Rong-Yaun0Wang Chun-Hua1Wu Chang-Chieh2Wang Lu-Kai3Tsai Fu-Ming4Department of Internal Medicine, Taipei Tzu Chi Hospital, The Buddhist Tzu Chi Medical Foundation, New Taipei City, TaiwanDepartment of Dermatology, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City, Taiwan + School of Medicine, Tzu Chi University, Hualien, TaiwanDepartment of Surgery, Tri-Service General Hospital Keelung Branch, National Defense Medical Center, Keelung, TaiwanDepartment of Life Sciences, National Science and Technology Council, Taipei, TaiwanDepartment of Research, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City, TaiwanGastric cancer is a commonly diagnosed form of cancer, and cisplatin is commonly used as a chemotherapy drug for treating it. However, the side effects of cisplatin may reduce patients’ willingness to use it. Seselin, a derivative of coumarin, has been found to have anticancer properties as well as anticoagulant effects. In this study, we investigated the effect of seselin on promoting cisplatin-induced gastric cancer cell death using the cell proliferation reagent WST-1, BrdU incorporation and lactate dehydrogenase release. The role of seselin and cisplatin in the apoptosis of gastric cancer cells was analyzed using a phospho-kinase array and Western blot analysis. Seselin did not affect G2/M stasis, but it promoted cell death in AGS cells treated with cisplatin. Phospho-kinase array analysis revealed that cisplatin regulates intracellular p53 phosphorylation, while seselin regulates intracellular β-catenin expression by affecting the phosphorylation of glycogen synthase kinase-3 beta (GSK-3β), extracellular-signal-regulated kinase (ERK) and Src tyrosine kinase. Seselin and cisplatin promote the apoptosis of gastric cancer cells by the synergistic effect of two distinct signaling pathways. These findings suggest that seselin may be used as a complementary therapy to reduce the clinical dose of chemotherapy.https://doiserbia.nb.rs/img/doi/0354-4664/2023/0354-46642300023S.pdfseselincisplatincoumarinapoptosiscomplementary therapy
spellingShingle Shyu Rong-Yaun
Wang Chun-Hua
Wu Chang-Chieh
Wang Lu-Kai
Tsai Fu-Ming
Seselin promotes cisplatin-induced apoptosis of AGS gastric cancer cells by inhibiting β-catenin expression
Archives of Biological Sciences
seselin
cisplatin
coumarin
apoptosis
complementary therapy
title Seselin promotes cisplatin-induced apoptosis of AGS gastric cancer cells by inhibiting β-catenin expression
title_full Seselin promotes cisplatin-induced apoptosis of AGS gastric cancer cells by inhibiting β-catenin expression
title_fullStr Seselin promotes cisplatin-induced apoptosis of AGS gastric cancer cells by inhibiting β-catenin expression
title_full_unstemmed Seselin promotes cisplatin-induced apoptosis of AGS gastric cancer cells by inhibiting β-catenin expression
title_short Seselin promotes cisplatin-induced apoptosis of AGS gastric cancer cells by inhibiting β-catenin expression
title_sort seselin promotes cisplatin induced apoptosis of ags gastric cancer cells by inhibiting β catenin expression
topic seselin
cisplatin
coumarin
apoptosis
complementary therapy
url https://doiserbia.nb.rs/img/doi/0354-4664/2023/0354-46642300023S.pdf
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