Investigating the regulation mechanism of baicalin on triple negative breast cancer’s biological network by a systematic biological strategy

Yang, Kailin; Zeng, Liuting; Ge, Anqi; Chen, Zhouhua; Bao, Tingting; Long, Zhiyong; Ge, Jinwen; Li-zhong, Huang

doi:10.1016/j.biopha.2019.109253

Cited by 22 publications

(33 citation statements)

References 62 publications

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“…(Lin et al, 2018) is a commonly used database. Oral bioavailability (OB), Caco-2 permeability and drug-likeness (DL) were utilized to identify the potential bioactive compounds of XHP (Walters and Murcko, 2002;Ano et al, 2004;Hu et al, 2009;Xu et al, 2012;Zeng and Yang, 2017;Yang et al, 2018;Yang et al, 2019). The compounds with OB ≥30%, Caco-2 > −0.4 and DL ≥0.18 were regard as oral absorbable compounds with biologically active (Walters and Murcko, 2002;Ano et al, 2004;Hu et al, 2009;Xu et al, 2012;Zeng and Yang, 2017;Yang et al, 2018;Yang et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

“…Although the above studies have described some of the mechanisms of XHP against TNBC, the mechanism remains unclear. In our previous studies, we successfully used multiple bioinformatics techniques and transcriptomics to analyze the mechanisms by which traditional Chinese Medicine interferes with different types of breast cancer (Zeng and Yang, 2017;Yang et al, 2018;Yang et al, 2019). Therefore, this study will use a multi-directional pharmacology strategy based on chemical informatics and transcriptomics to clarify the mechanisms by which XHP and Olibanum treat TNBC.…”

Section: Introductionmentioning

confidence: 99%

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Exploring the Regulation Mechanism of Xihuang Pill, Olibanum and β-Boswellic Acid on the Biomolecular Network of Triple-Negative Breast Cancer Based on Transcriptomics and Chemical Informatics Methodology

Yang

Zeng

et al. 2020

Front. Pharmacol.

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Background: Xihuang Pill (XHP) is mainly used to treat "Ru Yan (breast cancer)". Evidence-based medical evidence and showed that XHP improves the efficacy of chemotherapy and reduced chemotherapy-induced toxicity in breast cancer patients. However, the mechanism of XHP against breast cancer is not clear. Methods: The effect of XHP extract on cell half-inhibitory concentration (IC50) and cell viability of MD-MB-231 cells was detected by CCK-8 method. The cell inhibition rate of MDA-MB-453 cells were detected by MTT method. Apoptosis was detected by flow cytometry, cell transfer ability was detected by Transwell method, and cell proliferation ability was detected by colony formation assay. The expression of Notch1, b-catenin and c-myc mRNA in MDA-MB-453 cells were detected by real-time fluorescence quantitative PCR. Then, chemical informatics and transcriptomics methodology was utilized to predict the potential compounds and targets of XHP, and collect triple negative breast cancer (TNBC) genes and the data of Olibanum and b-boswellic acid intervention MD-MB-231 cells (from GSE102891). The cytoscape software was utilized to undergo network construction and network analysis. Finally, the data from the network analysis was imported into the DAVID database for enrichment analysis of signaling pathways and biological processes. Results: The IC50 was 15.08 g/L (for MD-MB-231 cells). After interfering with MD-MB-231 cells with 15.08 g/L XHP extract for 72 h, compared with the control group, the cell viability, migration and proliferation was significantly decreased, while early apoptosis and

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Exploring the Regulation Mechanism of Xihuang Pill, Olibanum and β-Boswellic Acid on the Biomolecular Network of Triple-Negative Breast Cancer Based on Transcriptomics and Chemical Informatics Methodology

Yang

Zeng

et al. 2020

Front. Pharmacol.

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“…Construct the following networks:(1) Cluster 1 for non-small cell lung cancer network; (2) Fucosterol-NSCLC candidate targets PPI network; (3) important biological processes and candidate targets crosstalk network; (4) KEGG pathway and candidate targets crosstalk network Cluster for NSCLC network The disease module is a set of network components that collectively disrupts cellular function and lead to a specific disease phenotype. Owing to the disease module, the functional module and the topology module have the same meaning in the network, the function module is equal to the topology module, and the disease can be can be considered as interference and destruction of functional module [30,31].The plug-in MCODE of Cytoscape3.7.2 software was used to analyze the protein interaction network of non-small cell lung cancer to find the dense regions, and the first cluster of results was retained.…”

Section: Network Construction Network Construction Methodsmentioning

confidence: 99%

Exploration in the mechanism of fucosterol for the treatment of non-small cell lung cancer Based on network pharmacology and molecular docking

Lin

et al. 2020

Preprint

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Background: It has been demonstrated that fucosterol induces a therapeutic effect on cancer. However, the molecular mechanisms underlying the effects of fucosterol in the treatment of non-small cell lung cancer are still unclear.Methods: In this study, pharmMapper and GeneCards databases were utilized to gather the prediction of fucosterol targets and NSCLC-related targets. The mechanisms of fucosterol against NSCLC were identified in DAVID6.8 by enrichment analysis of GO and KEGG, and protein-protein interaction data was obtained from Sting Database. Molecular docking was used to predict the docking of GRB2. Moreover, the relationship of GRB2 expression and immune infiltrates was analyzed by TIMER database.Results: The results suggest that fucosterol acts against by candidate targets, such as MAPK1, EGFR, GRB2, IGF2, MAPK8 and SRC, which regulate biological processes including negative regulation of apoptotic process, peptidyl-tyrosine phosphorylation, positive regulation of cell proliferation. The Raf / MEK / ERK signaling pathway initiated by GRB2 maybe the most significant pathway for fucosterol to treat NSCLC.Conclusions: These results show that GRB2 is the key target for fucosterol in the treatment of NSCLC, which laying a theoretical foundation for further research and providing scientific support for the development of new drugs.

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“…The disease module is a set of network components that collectively disrupts cellular function and lead to a speci c disease phenotype. Owing to the disease module, the functional module and the topology module have the same meaning in the network, the function module is equal to the topology module, and the disease can be can be considered as interference and destruction of functional module [30,31].The plug-in MCODE of Cytoscape3.7.2 software was used to analyze the protein interaction network of nonsmall cell lung cancer to nd the dense regions, and the rst cluster of results was retained.…”

Section: Protein-protein Interaction Datamentioning

confidence: 99%

Exploration in the mechanism of fucosterol for the treatment of non-small cell lung cancer based on network pharmacology and molecular docking

Lin

et al. 2020

Preprint

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Background It has been demonstrated that fucosterol induces a therapeutic effect on cancer. However, the molecular mechanisms underlying the effects of fucosterol in the treatment of non-small cell lung cancer are still unclear.Methods In this study, pharmMapper and GeneCards databases were utilized to gather the prediction of fucosterol targets and NSCLC-related targets. The mechanisms of fucosterol against NSCLC were identified in DAVID6.8 by enrichment analysis of GO and KEGG, and protein-protein interaction data was obtained from Sting Database. Molecular docking was used to predict the docking of GRB2. Moreover, the relationship of GRB2 expression and immune infiltrates was analyzed by TIMER database.Results The results suggest that fucosterol acts against by candidate targets, such as MAPK1, EGFR, GRB2, IGF2, MAPK8 and SRC, which regulate biological processes including negative regulation of apoptotic process, peptidyl-tyrosine phosphorylation, positive regulation of cell proliferation. The Raf / MEK / ERK signaling pathway initiated by GRB2 maybe the most significant pathway for fucosterol to treat NSCLC.Conclusions These results show that GRB2 is the key target for fucosterol in the treatment of NSCLC, which laying a theoretical foundation for further research and providing scientific support for the development of new drugs.

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Investigating the regulation mechanism of baicalin on triple negative breast cancer’s biological network by a systematic biological strategy

Cited by 22 publications

References 62 publications

Exploring the Regulation Mechanism of Xihuang Pill, Olibanum and β-Boswellic Acid on the Biomolecular Network of Triple-Negative Breast Cancer Based on Transcriptomics and Chemical Informatics Methodology

Exploring the Regulation Mechanism of Xihuang Pill, Olibanum and β-Boswellic Acid on the Biomolecular Network of Triple-Negative Breast Cancer Based on Transcriptomics and Chemical Informatics Methodology

Exploration in the mechanism of fucosterol for the treatment of non-small cell lung cancer Based on network pharmacology and molecular docking

Exploration in the mechanism of fucosterol for the treatment of non-small cell lung cancer based on network pharmacology and molecular docking

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