Ghrelin Regulates Cyclooxygenase-2 Expression and Promotes Gastric Cancer Cell Progression
Aim. To research the molecular mechanism of ghrelin in apoptosis, migratory, and invasion of gastric cancer (GC) cells. Methods. After GC AGS cells were handled with ghrelin (10–8 M), cyclooxygenase-2 inhibitor NS398 (100 μM), and Akt inhibitor perifosine (10uM), the rates of apoptosis were detected...
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2021-01-01
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Series: | Computational and Mathematical Methods in Medicine |
Online Access: | http://dx.doi.org/10.1155/2021/5576808 |
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doaj-518cf2e9b0ed4f1e9002231f6643b4692021-06-07T02:14:15ZengHindawi LimitedComputational and Mathematical Methods in Medicine1748-67182021-01-01202110.1155/2021/5576808Ghrelin Regulates Cyclooxygenase-2 Expression and Promotes Gastric Cancer Cell ProgressionHuanqing Li0Xiaohong Zhang1Li Feng2Endoscopy CenterEndoscopy CenterEndoscopy CenterAim. To research the molecular mechanism of ghrelin in apoptosis, migratory, and invasion of gastric cancer (GC) cells. Methods. After GC AGS cells were handled with ghrelin (10–8 M), cyclooxygenase-2 inhibitor NS398 (100 μM), and Akt inhibitor perifosine (10uM), the rates of apoptosis were detected by TUNEL assay and flow cytometry assay. We assessed the expressions of PI3K, p-Akt, and COX-2 proteins by making use of Western blot analysis. The cell migratory and invasion were detected by using wound-healing and transwell analysis. Results. The migratory and invasion were increased in ghrelin-treated cells, while the rates of apoptosis were decreased. GC AGS cells treated with ghrelin showed an increase in protein expression of p-Akt, PI3K, and COX-2. After cells were treated with Akt inhibitor perifosine, the protein expression of p-Akt, PI3K, and COX-2 and the cell migratory, invasion, and apoptosis were partly recovered. After cells were treated with cyclooxygenase-2 inhibitor NS398, the protein expression of COX-2 and the cell migratory and invasion were decreased, while the rates of apoptosis were increased. Conclusion. Ghrelin regulates cell migration, invasion, and apoptosis in GC cells through targeting PI3K/Akt/COX-2. Ghrelin increases the expression of COX-2 in GC cells by targeting PI3K/Akt. Ghrelin is suggested to be one of the molecular targets in GC.http://dx.doi.org/10.1155/2021/5576808 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Huanqing Li Xiaohong Zhang Li Feng |
spellingShingle |
Huanqing Li Xiaohong Zhang Li Feng Ghrelin Regulates Cyclooxygenase-2 Expression and Promotes Gastric Cancer Cell Progression Computational and Mathematical Methods in Medicine |
author_facet |
Huanqing Li Xiaohong Zhang Li Feng |
author_sort |
Huanqing Li |
title |
Ghrelin Regulates Cyclooxygenase-2 Expression and Promotes Gastric Cancer Cell Progression |
title_short |
Ghrelin Regulates Cyclooxygenase-2 Expression and Promotes Gastric Cancer Cell Progression |
title_full |
Ghrelin Regulates Cyclooxygenase-2 Expression and Promotes Gastric Cancer Cell Progression |
title_fullStr |
Ghrelin Regulates Cyclooxygenase-2 Expression and Promotes Gastric Cancer Cell Progression |
title_full_unstemmed |
Ghrelin Regulates Cyclooxygenase-2 Expression and Promotes Gastric Cancer Cell Progression |
title_sort |
ghrelin regulates cyclooxygenase-2 expression and promotes gastric cancer cell progression |
publisher |
Hindawi Limited |
series |
Computational and Mathematical Methods in Medicine |
issn |
1748-6718 |
publishDate |
2021-01-01 |
description |
Aim. To research the molecular mechanism of ghrelin in apoptosis, migratory, and invasion of gastric cancer (GC) cells. Methods. After GC AGS cells were handled with ghrelin (10–8 M), cyclooxygenase-2 inhibitor NS398 (100 μM), and Akt inhibitor perifosine (10uM), the rates of apoptosis were detected by TUNEL assay and flow cytometry assay. We assessed the expressions of PI3K, p-Akt, and COX-2 proteins by making use of Western blot analysis. The cell migratory and invasion were detected by using wound-healing and transwell analysis. Results. The migratory and invasion were increased in ghrelin-treated cells, while the rates of apoptosis were decreased. GC AGS cells treated with ghrelin showed an increase in protein expression of p-Akt, PI3K, and COX-2. After cells were treated with Akt inhibitor perifosine, the protein expression of p-Akt, PI3K, and COX-2 and the cell migratory, invasion, and apoptosis were partly recovered. After cells were treated with cyclooxygenase-2 inhibitor NS398, the protein expression of COX-2 and the cell migratory and invasion were decreased, while the rates of apoptosis were increased. Conclusion. Ghrelin regulates cell migration, invasion, and apoptosis in GC cells through targeting PI3K/Akt/COX-2. Ghrelin increases the expression of COX-2 in GC cells by targeting PI3K/Akt. Ghrelin is suggested to be one of the molecular targets in GC. |
url |
http://dx.doi.org/10.1155/2021/5576808 |
work_keys_str_mv |
AT huanqingli ghrelinregulatescyclooxygenase2expressionandpromotesgastriccancercellprogression AT xiaohongzhang ghrelinregulatescyclooxygenase2expressionandpromotesgastriccancercellprogression AT lifeng ghrelinregulatescyclooxygenase2expressionandpromotesgastriccancercellprogression |
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