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Hyperin Controls the Development and Therapy of Gastric Cancer via Regulating Wnt/β-Catenin Signaling
BACKGROUND: Hyperin is an effective monomer extracted from Malvaceae plant Abelmoschus, which is a flavonol glycoside compound. Hyperin performs a variety of pharmacological activities, such as analgesia, antioxidation, anti-inflammation, avoiding microthrombosis, regulating immune function, inhibit...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Dove
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7680131/ https://www.ncbi.nlm.nih.gov/pubmed/33235505 http://dx.doi.org/10.2147/CMAR.S270544 |
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author | Ping, Mao-Hua |
author_facet | Ping, Mao-Hua |
author_sort | Ping, Mao-Hua |
collection | PubMed |
description | BACKGROUND: Hyperin is an effective monomer extracted from Malvaceae plant Abelmoschus, which is a flavonol glycoside compound. Hyperin performs a variety of pharmacological activities, such as analgesia, antioxidation, anti-inflammation, avoiding microthrombosis, regulating immune function, inhibiting tumor cell growth. But the role of Hyperin on gastric cancer is unrevealed. Considering the essential role of Hyperin, Hyperin function in gastric cancer is necessary to explore. AIM: To identify the function of Hyperin in gastric cancer. METHODS: The role of Hyperin on gastric cell progression was detected in our research. Proliferation, migration, and invasion ability were assessed by the CCK-8, colony formation, cell-cycle assay, wound healing, Transwell migration and invasion assays. TUNEL assay and flow cytometry showed the results of the apoptosis level. Further, caspase-3, -9 activity and apoptosis-associated protein were assessed by the Caspase activity kit and Western blot. Wnt/β-catenin signal pathway activity was appraised by TOP/FOP luciferase activity. Immunohistochemical staining was performed to detect the role of Hyperin on tumor growth in vivo. RESULTS: Functional experiments showed that Hyperin inhibited proliferation, migration, and invasion and induced apoptosis in gastric cancer cells. Meanwhile, Hyperin prevented tumor growth by suppressing Wnt/β-catenin signal pathway. CONCLUSION: The present study revealed that Hyperin suppressed gastric cancer progression by controlling Wnt/β-catenin signal pathway, which provided a novel therapy in gastric cancer. |
format | Online Article Text |
id | pubmed-7680131 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-76801312020-11-23 Hyperin Controls the Development and Therapy of Gastric Cancer via Regulating Wnt/β-Catenin Signaling Ping, Mao-Hua Cancer Manag Res Original Research BACKGROUND: Hyperin is an effective monomer extracted from Malvaceae plant Abelmoschus, which is a flavonol glycoside compound. Hyperin performs a variety of pharmacological activities, such as analgesia, antioxidation, anti-inflammation, avoiding microthrombosis, regulating immune function, inhibiting tumor cell growth. But the role of Hyperin on gastric cancer is unrevealed. Considering the essential role of Hyperin, Hyperin function in gastric cancer is necessary to explore. AIM: To identify the function of Hyperin in gastric cancer. METHODS: The role of Hyperin on gastric cell progression was detected in our research. Proliferation, migration, and invasion ability were assessed by the CCK-8, colony formation, cell-cycle assay, wound healing, Transwell migration and invasion assays. TUNEL assay and flow cytometry showed the results of the apoptosis level. Further, caspase-3, -9 activity and apoptosis-associated protein were assessed by the Caspase activity kit and Western blot. Wnt/β-catenin signal pathway activity was appraised by TOP/FOP luciferase activity. Immunohistochemical staining was performed to detect the role of Hyperin on tumor growth in vivo. RESULTS: Functional experiments showed that Hyperin inhibited proliferation, migration, and invasion and induced apoptosis in gastric cancer cells. Meanwhile, Hyperin prevented tumor growth by suppressing Wnt/β-catenin signal pathway. CONCLUSION: The present study revealed that Hyperin suppressed gastric cancer progression by controlling Wnt/β-catenin signal pathway, which provided a novel therapy in gastric cancer. Dove 2020-11-17 /pmc/articles/PMC7680131/ /pubmed/33235505 http://dx.doi.org/10.2147/CMAR.S270544 Text en © 2020 Ping. 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 Ping, Mao-Hua Hyperin Controls the Development and Therapy of Gastric Cancer via Regulating Wnt/β-Catenin Signaling |
title | Hyperin Controls the Development and Therapy of Gastric Cancer via Regulating Wnt/β-Catenin Signaling |
title_full | Hyperin Controls the Development and Therapy of Gastric Cancer via Regulating Wnt/β-Catenin Signaling |
title_fullStr | Hyperin Controls the Development and Therapy of Gastric Cancer via Regulating Wnt/β-Catenin Signaling |
title_full_unstemmed | Hyperin Controls the Development and Therapy of Gastric Cancer via Regulating Wnt/β-Catenin Signaling |
title_short | Hyperin Controls the Development and Therapy of Gastric Cancer via Regulating Wnt/β-Catenin Signaling |
title_sort | hyperin controls the development and therapy of gastric cancer via regulating wnt/β-catenin signaling |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7680131/ https://www.ncbi.nlm.nih.gov/pubmed/33235505 http://dx.doi.org/10.2147/CMAR.S270544 |
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