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The Potential Mechanisms of Cinobufotalin Treating Colon Adenocarcinoma by Network Pharmacology

Network pharmacology, as a novel way using bioinformatics to explore drug targets and interactions in cancer, broadens our understanding of drug action, thereby facilitating drug discovery. Here, we utilized network pharmacology to explore the role and mechanism by which cinobufotalin functions in c...

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Autores principales: Wang, Jiyan, Chang, Hongkai, Su, Meng, Zhao, Huifang, Qiao, Yaya, Wang, Yu, Shang, Luqing, Shan, Changliang, Zhang, Shuai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9262105/
https://www.ncbi.nlm.nih.gov/pubmed/35814224
http://dx.doi.org/10.3389/fphar.2022.934729
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author Wang, Jiyan
Chang, Hongkai
Su, Meng
Zhao, Huifang
Qiao, Yaya
Wang, Yu
Shang, Luqing
Shan, Changliang
Zhang, Shuai
author_facet Wang, Jiyan
Chang, Hongkai
Su, Meng
Zhao, Huifang
Qiao, Yaya
Wang, Yu
Shang, Luqing
Shan, Changliang
Zhang, Shuai
author_sort Wang, Jiyan
collection PubMed
description Network pharmacology, as a novel way using bioinformatics to explore drug targets and interactions in cancer, broadens our understanding of drug action, thereby facilitating drug discovery. Here, we utilized network pharmacology to explore the role and mechanism by which cinobufotalin functions in colon adenocarcinoma (COAD). We found that cinobufotalin represses the growth and proliferation of colon cancer cells, and integrated public databases for targets reported to be associated with COAD, together with those predicted to be targets of cinobufotalin. Targets overlapped between COAD-associated proteins and cinobufotalin target proteins were used to filter candidate targets of cinobufotalin in COAD. The following proteins were thought to occupy a key position in COAD-cinobufotalin target networks: SRC, PIK3R1, MAPK1, PIK3CA, HSP90AA1, CTNNB1, GRB2, RHO1, PTPN11, and EGFR. The networks regulated by cinobufotalin were involved mainly in extracellular signal stimulation and transduction, including MAPK signaling pathway, PI3K-AKT signaling pathway, and JAK-STAT signaling pathway. Besides, transcriptome sequencing results also indicated that cinobufotalin inhibits the response of colon cancer cells to extracellular stimulation and promotes cell apoptosis. Molecular docking results showed that cinobufotalin matches in the pocket of the top candidate cinobufotalin target proteins (SRC, PIK3R1, MAPK1 and PIK3CA). These findings demonstrate cinobufotalin can be developed as potential anti-cancer therapeutics.
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spelling pubmed-92621052022-07-08 The Potential Mechanisms of Cinobufotalin Treating Colon Adenocarcinoma by Network Pharmacology Wang, Jiyan Chang, Hongkai Su, Meng Zhao, Huifang Qiao, Yaya Wang, Yu Shang, Luqing Shan, Changliang Zhang, Shuai Front Pharmacol Pharmacology Network pharmacology, as a novel way using bioinformatics to explore drug targets and interactions in cancer, broadens our understanding of drug action, thereby facilitating drug discovery. Here, we utilized network pharmacology to explore the role and mechanism by which cinobufotalin functions in colon adenocarcinoma (COAD). We found that cinobufotalin represses the growth and proliferation of colon cancer cells, and integrated public databases for targets reported to be associated with COAD, together with those predicted to be targets of cinobufotalin. Targets overlapped between COAD-associated proteins and cinobufotalin target proteins were used to filter candidate targets of cinobufotalin in COAD. The following proteins were thought to occupy a key position in COAD-cinobufotalin target networks: SRC, PIK3R1, MAPK1, PIK3CA, HSP90AA1, CTNNB1, GRB2, RHO1, PTPN11, and EGFR. The networks regulated by cinobufotalin were involved mainly in extracellular signal stimulation and transduction, including MAPK signaling pathway, PI3K-AKT signaling pathway, and JAK-STAT signaling pathway. Besides, transcriptome sequencing results also indicated that cinobufotalin inhibits the response of colon cancer cells to extracellular stimulation and promotes cell apoptosis. Molecular docking results showed that cinobufotalin matches in the pocket of the top candidate cinobufotalin target proteins (SRC, PIK3R1, MAPK1 and PIK3CA). These findings demonstrate cinobufotalin can be developed as potential anti-cancer therapeutics. Frontiers Media S.A. 2022-06-23 /pmc/articles/PMC9262105/ /pubmed/35814224 http://dx.doi.org/10.3389/fphar.2022.934729 Text en Copyright © 2022 Wang, Chang, Su, Zhao, Qiao, Wang, Shang, Shan and Zhang. 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 Pharmacology
Wang, Jiyan
Chang, Hongkai
Su, Meng
Zhao, Huifang
Qiao, Yaya
Wang, Yu
Shang, Luqing
Shan, Changliang
Zhang, Shuai
The Potential Mechanisms of Cinobufotalin Treating Colon Adenocarcinoma by Network Pharmacology
title The Potential Mechanisms of Cinobufotalin Treating Colon Adenocarcinoma by Network Pharmacology
title_full The Potential Mechanisms of Cinobufotalin Treating Colon Adenocarcinoma by Network Pharmacology
title_fullStr The Potential Mechanisms of Cinobufotalin Treating Colon Adenocarcinoma by Network Pharmacology
title_full_unstemmed The Potential Mechanisms of Cinobufotalin Treating Colon Adenocarcinoma by Network Pharmacology
title_short The Potential Mechanisms of Cinobufotalin Treating Colon Adenocarcinoma by Network Pharmacology
title_sort potential mechanisms of cinobufotalin treating colon adenocarcinoma by network pharmacology
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9262105/
https://www.ncbi.nlm.nih.gov/pubmed/35814224
http://dx.doi.org/10.3389/fphar.2022.934729
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