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Review of molecular biological studies on acute lymphoblastic leukemia treated by modified shengmaiyin

The objective was to explore the pharmacological mechanism of modified shengmaiyin (MSMY) in the treatment of acute lymphoblastic leukemia (ALL) by network pharmacology analysis. The effective components and predicted targets of MSMY were collected from TCMSP and Swiss target prediction databases, a...

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Autores principales: Guo, Dongyu, Gu, Mengyu, Du, Fuquan, Zhao, Yuting, Gao, Mingjie, Hao, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10256333/
https://www.ncbi.nlm.nih.gov/pubmed/37335634
http://dx.doi.org/10.1097/MD.0000000000034013
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author Guo, Dongyu
Gu, Mengyu
Du, Fuquan
Zhao, Yuting
Gao, Mingjie
Hao, Jing
author_facet Guo, Dongyu
Gu, Mengyu
Du, Fuquan
Zhao, Yuting
Gao, Mingjie
Hao, Jing
author_sort Guo, Dongyu
collection PubMed
description The objective was to explore the pharmacological mechanism of modified shengmaiyin (MSMY) in the treatment of acute lymphoblastic leukemia (ALL) by network pharmacology analysis. The effective components and predicted targets of MSMY were collected from TCMSP and Swiss target prediction databases, and the related targets of ALL were screened by GeneCards and DisGeNET. The core targets and related signaling pathways of MSMY active ingredients for the treatment of ALL were predicted by protein-protein interaction network (PPI), gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis. We identified 172 potential targets for the active components of MSMY, 538 disease targets associated with ALL, and 59 common gene targets. PPI network showed that 27 targets such as triptolide, RAC-alpha serine/threonine-protein kinase (AKT1), vascular endothelial growth factor A and Caspase-3 (CASP3) were the core targets. KEGG enrichment analysis related signaling pathways included cancer pathway, phosphatidylinositol 3 kinase, PI-3K/protein kinase B (PI3K-Akt) signaling pathway, apoptosis and mitogen-activated protein kinase (MAPK) signaling pathway and IL-17 signaling pathway. The effective active components and potential therapeutic targets of MSMY in the treatment of ALL were initially identified by comprehensive network pharmacology, which provides a theoretical basis for further study of the material basis and molecular mechanism of MSMY in the treatment of ALL.
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spelling pubmed-102563332023-06-10 Review of molecular biological studies on acute lymphoblastic leukemia treated by modified shengmaiyin Guo, Dongyu Gu, Mengyu Du, Fuquan Zhao, Yuting Gao, Mingjie Hao, Jing Medicine (Baltimore) 3800 The objective was to explore the pharmacological mechanism of modified shengmaiyin (MSMY) in the treatment of acute lymphoblastic leukemia (ALL) by network pharmacology analysis. The effective components and predicted targets of MSMY were collected from TCMSP and Swiss target prediction databases, and the related targets of ALL were screened by GeneCards and DisGeNET. The core targets and related signaling pathways of MSMY active ingredients for the treatment of ALL were predicted by protein-protein interaction network (PPI), gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis. We identified 172 potential targets for the active components of MSMY, 538 disease targets associated with ALL, and 59 common gene targets. PPI network showed that 27 targets such as triptolide, RAC-alpha serine/threonine-protein kinase (AKT1), vascular endothelial growth factor A and Caspase-3 (CASP3) were the core targets. KEGG enrichment analysis related signaling pathways included cancer pathway, phosphatidylinositol 3 kinase, PI-3K/protein kinase B (PI3K-Akt) signaling pathway, apoptosis and mitogen-activated protein kinase (MAPK) signaling pathway and IL-17 signaling pathway. The effective active components and potential therapeutic targets of MSMY in the treatment of ALL were initially identified by comprehensive network pharmacology, which provides a theoretical basis for further study of the material basis and molecular mechanism of MSMY in the treatment of ALL. Lippincott Williams & Wilkins 2023-06-09 /pmc/articles/PMC10256333/ /pubmed/37335634 http://dx.doi.org/10.1097/MD.0000000000034013 Text en Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY) (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle 3800
Guo, Dongyu
Gu, Mengyu
Du, Fuquan
Zhao, Yuting
Gao, Mingjie
Hao, Jing
Review of molecular biological studies on acute lymphoblastic leukemia treated by modified shengmaiyin
title Review of molecular biological studies on acute lymphoblastic leukemia treated by modified shengmaiyin
title_full Review of molecular biological studies on acute lymphoblastic leukemia treated by modified shengmaiyin
title_fullStr Review of molecular biological studies on acute lymphoblastic leukemia treated by modified shengmaiyin
title_full_unstemmed Review of molecular biological studies on acute lymphoblastic leukemia treated by modified shengmaiyin
title_short Review of molecular biological studies on acute lymphoblastic leukemia treated by modified shengmaiyin
title_sort review of molecular biological studies on acute lymphoblastic leukemia treated by modified shengmaiyin
topic 3800
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10256333/
https://www.ncbi.nlm.nih.gov/pubmed/37335634
http://dx.doi.org/10.1097/MD.0000000000034013
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