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The feasibility of using the compound kushen injection to treat cervical cancer based on network pharmacology and transcriptomics
BACKGROUND: To investigate the molecular targets and mechanisms of compound kushen injection (CKI) in the prevention and treatment of cervical cancer based on network pharmacology and transcriptomics. METHODS: In this study, we used network pharmacology methods to screen for effective compounds, int...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Lippincott Williams & Wilkins
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10489532/ https://www.ncbi.nlm.nih.gov/pubmed/37682145 http://dx.doi.org/10.1097/MD.0000000000035135 |
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author | Zhang, Yiting Xu, Linjing Li, Ling |
author_facet | Zhang, Yiting Xu, Linjing Li, Ling |
author_sort | Zhang, Yiting |
collection | PubMed |
description | BACKGROUND: To investigate the molecular targets and mechanisms of compound kushen injection (CKI) in the prevention and treatment of cervical cancer based on network pharmacology and transcriptomics. METHODS: In this study, we used network pharmacology methods to screen for effective compounds, integrated the results of network pharmacology and RNA-seq to comprehensively screen and predict target genes, analyze the biological functions and signaling pathways of target genes, and construct a PPI network to screen for hub genes. The results were further verified by biological experiments, molecular docking, RT-PCR, and western blot analysis. RESULTS: The results showed that the hub genes CXCL2, anti-vascular endothelial growth factor, hexokinase 2 are therapeutic targets of CKI for the treatment of Cervical Cancer. These targets were significantly enriched in pathways mainly including pathways in cancer, cell cycle, MAPK signaling pathways, etc. In vitro cell experiments showed that CKI could effectively inhibit the proliferation of cancer cells, promote apoptosis, and induce cell cycle arrest. RT-PCR and western blot experiments showed that the expression of hub genes was significantly decreased. The compounds have good binding activity to hub genes. CONCLUSION: CKI, based on its active ingredients and through multiple targets and multiple pathways, can stop the growth of cervical cancer cells at a certain phase of the cell cycle and cause apoptosis, which proved CKI’s effect in treating cervical cancer. |
format | Online Article Text |
id | pubmed-10489532 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Lippincott Williams & Wilkins |
record_format | MEDLINE/PubMed |
spelling | pubmed-104895322023-09-09 The feasibility of using the compound kushen injection to treat cervical cancer based on network pharmacology and transcriptomics Zhang, Yiting Xu, Linjing Li, Ling Medicine (Baltimore) 5700 BACKGROUND: To investigate the molecular targets and mechanisms of compound kushen injection (CKI) in the prevention and treatment of cervical cancer based on network pharmacology and transcriptomics. METHODS: In this study, we used network pharmacology methods to screen for effective compounds, integrated the results of network pharmacology and RNA-seq to comprehensively screen and predict target genes, analyze the biological functions and signaling pathways of target genes, and construct a PPI network to screen for hub genes. The results were further verified by biological experiments, molecular docking, RT-PCR, and western blot analysis. RESULTS: The results showed that the hub genes CXCL2, anti-vascular endothelial growth factor, hexokinase 2 are therapeutic targets of CKI for the treatment of Cervical Cancer. These targets were significantly enriched in pathways mainly including pathways in cancer, cell cycle, MAPK signaling pathways, etc. In vitro cell experiments showed that CKI could effectively inhibit the proliferation of cancer cells, promote apoptosis, and induce cell cycle arrest. RT-PCR and western blot experiments showed that the expression of hub genes was significantly decreased. The compounds have good binding activity to hub genes. CONCLUSION: CKI, based on its active ingredients and through multiple targets and multiple pathways, can stop the growth of cervical cancer cells at a certain phase of the cell cycle and cause apoptosis, which proved CKI’s effect in treating cervical cancer. Lippincott Williams & Wilkins 2023-09-08 /pmc/articles/PMC10489532/ /pubmed/37682145 http://dx.doi.org/10.1097/MD.0000000000035135 Text en Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc. https://creativecommons.org/licenses/by-nc/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial License 4.0 (CCBY-NC) (https://creativecommons.org/licenses/by-nc/4.0/) , where it is permissible to download, share, remix, transform, and buildup the work provided it is properly cited. The work cannot be used commercially without permission from the journal. |
spellingShingle | 5700 Zhang, Yiting Xu, Linjing Li, Ling The feasibility of using the compound kushen injection to treat cervical cancer based on network pharmacology and transcriptomics |
title | The feasibility of using the compound kushen injection to treat cervical cancer based on network pharmacology and transcriptomics |
title_full | The feasibility of using the compound kushen injection to treat cervical cancer based on network pharmacology and transcriptomics |
title_fullStr | The feasibility of using the compound kushen injection to treat cervical cancer based on network pharmacology and transcriptomics |
title_full_unstemmed | The feasibility of using the compound kushen injection to treat cervical cancer based on network pharmacology and transcriptomics |
title_short | The feasibility of using the compound kushen injection to treat cervical cancer based on network pharmacology and transcriptomics |
title_sort | feasibility of using the compound kushen injection to treat cervical cancer based on network pharmacology and transcriptomics |
topic | 5700 |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10489532/ https://www.ncbi.nlm.nih.gov/pubmed/37682145 http://dx.doi.org/10.1097/MD.0000000000035135 |
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