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Mechanism of action of icaritin on uterine corpus endometrial carcinoma based on network pharmacology and experimental evaluation
BACKGROUND: Uterine corpus endometrial carcinoma (UCEC) belongs to a group of epithelial malignant tumors. Icaritin is the main active compound of Epimedii Folium. Icaritin has been utilized to induce UCEC cells to death. METHODS: We wished to identify potential targets for icaritin in the treatment...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10394632/ https://www.ncbi.nlm.nih.gov/pubmed/37538114 http://dx.doi.org/10.3389/fonc.2023.1205604 |
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author | Jin, Yan-Bin Liang, Xiao-Chen Cai, Jun-Hong Wang, Kang Wang, Chen-Yang Wang, Wen-Hua Chen, Xiu-Li Bao, Shan |
author_facet | Jin, Yan-Bin Liang, Xiao-Chen Cai, Jun-Hong Wang, Kang Wang, Chen-Yang Wang, Wen-Hua Chen, Xiu-Li Bao, Shan |
author_sort | Jin, Yan-Bin |
collection | PubMed |
description | BACKGROUND: Uterine corpus endometrial carcinoma (UCEC) belongs to a group of epithelial malignant tumors. Icaritin is the main active compound of Epimedii Folium. Icaritin has been utilized to induce UCEC cells to death. METHODS: We wished to identify potential targets for icaritin in the treatment of UCEC, as well as to provide a groundwork for future studies into its pharmacologic mechanism of action. Network pharmacology was employed to conduct investigations on icaritin. Target proteins were chosen from the components of icaritin for UCEC treatment. A protein–protein interaction (PPI) network was established using overlapping genes. Analyses of enrichment of function and signaling pathways were undertaken using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases, respectively, to select “hub genes”. Finally, experiments were carried out to ascertain the effect of icaritin on endometrial cancer (HEC-1-A) cells. RESULTS: We demonstrated that icaritin has bioactive components and putative targets that are therapeutically important. Icaritin treatment induced sustained activation of the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt pathway) and inhibited growth of HEC-1-A cells. CONCLUSION: Our data provide a rationale for preclinical and clinical evaluations of icaritin for UCEC therapy. |
format | Online Article Text |
id | pubmed-10394632 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-103946322023-08-03 Mechanism of action of icaritin on uterine corpus endometrial carcinoma based on network pharmacology and experimental evaluation Jin, Yan-Bin Liang, Xiao-Chen Cai, Jun-Hong Wang, Kang Wang, Chen-Yang Wang, Wen-Hua Chen, Xiu-Li Bao, Shan Front Oncol Oncology BACKGROUND: Uterine corpus endometrial carcinoma (UCEC) belongs to a group of epithelial malignant tumors. Icaritin is the main active compound of Epimedii Folium. Icaritin has been utilized to induce UCEC cells to death. METHODS: We wished to identify potential targets for icaritin in the treatment of UCEC, as well as to provide a groundwork for future studies into its pharmacologic mechanism of action. Network pharmacology was employed to conduct investigations on icaritin. Target proteins were chosen from the components of icaritin for UCEC treatment. A protein–protein interaction (PPI) network was established using overlapping genes. Analyses of enrichment of function and signaling pathways were undertaken using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases, respectively, to select “hub genes”. Finally, experiments were carried out to ascertain the effect of icaritin on endometrial cancer (HEC-1-A) cells. RESULTS: We demonstrated that icaritin has bioactive components and putative targets that are therapeutically important. Icaritin treatment induced sustained activation of the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt pathway) and inhibited growth of HEC-1-A cells. CONCLUSION: Our data provide a rationale for preclinical and clinical evaluations of icaritin for UCEC therapy. Frontiers Media S.A. 2023-07-19 /pmc/articles/PMC10394632/ /pubmed/37538114 http://dx.doi.org/10.3389/fonc.2023.1205604 Text en Copyright © 2023 Jin, Liang, Cai, Wang, Wang, Wang, Chen and Bao https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Oncology Jin, Yan-Bin Liang, Xiao-Chen Cai, Jun-Hong Wang, Kang Wang, Chen-Yang Wang, Wen-Hua Chen, Xiu-Li Bao, Shan Mechanism of action of icaritin on uterine corpus endometrial carcinoma based on network pharmacology and experimental evaluation |
title | Mechanism of action of icaritin on uterine corpus endometrial carcinoma based on network pharmacology and experimental evaluation |
title_full | Mechanism of action of icaritin on uterine corpus endometrial carcinoma based on network pharmacology and experimental evaluation |
title_fullStr | Mechanism of action of icaritin on uterine corpus endometrial carcinoma based on network pharmacology and experimental evaluation |
title_full_unstemmed | Mechanism of action of icaritin on uterine corpus endometrial carcinoma based on network pharmacology and experimental evaluation |
title_short | Mechanism of action of icaritin on uterine corpus endometrial carcinoma based on network pharmacology and experimental evaluation |
title_sort | mechanism of action of icaritin on uterine corpus endometrial carcinoma based on network pharmacology and experimental evaluation |
topic | Oncology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10394632/ https://www.ncbi.nlm.nih.gov/pubmed/37538114 http://dx.doi.org/10.3389/fonc.2023.1205604 |
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