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Irisin functions to inhibit malignant growth of human pancreatic cancer cells via downregulation of the PI3K/AKT signaling pathway
INTRODUCTION: Irisin is a newly identified cytokine that has gained increasing attention because of its potential therapeutic applications in metabolic diseases and human cancers. Recently, accumulating evidence indicates that irisin plays an important role in the development and metastasis of vario...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6732507/ https://www.ncbi.nlm.nih.gov/pubmed/31564907 http://dx.doi.org/10.2147/OTT.S214260 |
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author | Zhang, Deguo Zhang, Ping Li, Luan Tang, Nan Huang, Fei Kong, Xianguo Tan, Xueying Shi, Guangjun |
author_facet | Zhang, Deguo Zhang, Ping Li, Luan Tang, Nan Huang, Fei Kong, Xianguo Tan, Xueying Shi, Guangjun |
author_sort | Zhang, Deguo |
collection | PubMed |
description | INTRODUCTION: Irisin is a newly identified cytokine that has gained increasing attention because of its potential therapeutic applications in metabolic diseases and human cancers. Recently, accumulating evidence indicates that irisin plays an important role in the development and metastasis of various tumors. The aim of this study was to evaluate the effects and underlying mechanisms of irisin on malignant growth of pancreatic cancer cells. MATERIALS AND METHODS: The anti-proliferative effect of irisin was examined using the CCK-8 assay. Irisin-induced apoptosis was determined by the annexin V-FITC/PI staining assay. The effects of irisin on cell migration and invasion were assessed using the scratch-induced wound healing assay and transwell invasion assay, respectively. The expression and phosphorylation of signaling proteins were detected by Western blot analysis. RESULTS: Our results showed that irisin inhibited cell proliferation and induced apoptosis of pancreatic cancer cells in a dose-dependent manner. In addition, irisin decreased the migration and invasion of pancreatic cancer cells. Finally, Western blot analysis revealed that irisin downregulated the PI3K/AKT signaling pathway. CONCLUSION: Our findings suggest that irisin is a novel therapeutic agent for pancreatic cancer. |
format | Online Article Text |
id | pubmed-6732507 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-67325072019-09-27 Irisin functions to inhibit malignant growth of human pancreatic cancer cells via downregulation of the PI3K/AKT signaling pathway Zhang, Deguo Zhang, Ping Li, Luan Tang, Nan Huang, Fei Kong, Xianguo Tan, Xueying Shi, Guangjun Onco Targets Ther Original Research INTRODUCTION: Irisin is a newly identified cytokine that has gained increasing attention because of its potential therapeutic applications in metabolic diseases and human cancers. Recently, accumulating evidence indicates that irisin plays an important role in the development and metastasis of various tumors. The aim of this study was to evaluate the effects and underlying mechanisms of irisin on malignant growth of pancreatic cancer cells. MATERIALS AND METHODS: The anti-proliferative effect of irisin was examined using the CCK-8 assay. Irisin-induced apoptosis was determined by the annexin V-FITC/PI staining assay. The effects of irisin on cell migration and invasion were assessed using the scratch-induced wound healing assay and transwell invasion assay, respectively. The expression and phosphorylation of signaling proteins were detected by Western blot analysis. RESULTS: Our results showed that irisin inhibited cell proliferation and induced apoptosis of pancreatic cancer cells in a dose-dependent manner. In addition, irisin decreased the migration and invasion of pancreatic cancer cells. Finally, Western blot analysis revealed that irisin downregulated the PI3K/AKT signaling pathway. CONCLUSION: Our findings suggest that irisin is a novel therapeutic agent for pancreatic cancer. Dove 2019-09-04 /pmc/articles/PMC6732507/ /pubmed/31564907 http://dx.doi.org/10.2147/OTT.S214260 Text en © 2019 Zhang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Zhang, Deguo Zhang, Ping Li, Luan Tang, Nan Huang, Fei Kong, Xianguo Tan, Xueying Shi, Guangjun Irisin functions to inhibit malignant growth of human pancreatic cancer cells via downregulation of the PI3K/AKT signaling pathway |
title | Irisin functions to inhibit malignant growth of human pancreatic cancer cells via downregulation of the PI3K/AKT signaling pathway |
title_full | Irisin functions to inhibit malignant growth of human pancreatic cancer cells via downregulation of the PI3K/AKT signaling pathway |
title_fullStr | Irisin functions to inhibit malignant growth of human pancreatic cancer cells via downregulation of the PI3K/AKT signaling pathway |
title_full_unstemmed | Irisin functions to inhibit malignant growth of human pancreatic cancer cells via downregulation of the PI3K/AKT signaling pathway |
title_short | Irisin functions to inhibit malignant growth of human pancreatic cancer cells via downregulation of the PI3K/AKT signaling pathway |
title_sort | irisin functions to inhibit malignant growth of human pancreatic cancer cells via downregulation of the pi3k/akt signaling pathway |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6732507/ https://www.ncbi.nlm.nih.gov/pubmed/31564907 http://dx.doi.org/10.2147/OTT.S214260 |
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