scholarly journals Transcriptome responses of intestinal epithelial cells induced by membrane vesicles of Listeria monocytogenes unveil novel insights into the host-pathogen cross talk

2019 ◽  
Author(s):  
Raman Karthikeyan ◽  
Pratapa Gayathri ◽  
Paramasamy Gunasekaran ◽  
Medicharla V. Jagannadham ◽  
Jeyaprakash Rajendhran
Keyword(s):  
Cell Cycle ◽  
Listeria Monocytogenes ◽  
Signaling Pathway ◽  
Mapk Pathway ◽  
Enrichment Analysis ◽  
Membrane Vesicles ◽  
Host Cells ◽  
Mitogen Activated Protein Kinase ◽  
Pathway Enrichment Analysis ◽  
Whole Cells

AbstractMembrane vesicles (MVs) serve as a vital source of virulence factors in many pathogenic organisms. The release of MVs by Listeria monocytogenes is only recently recognized, but its role in the pathogenesis is poorly understood. Here, we investigated the role of MVs of L. monocytogenes in virulence and host interactions. Proteomic analyses of whole cells and MVs of L. monocytogenes were performed using LC/MS/MS. A total of 1376 and 456 proteins were identified in the L. monocytogenes cells and MVs, respectively. Also, we have found that MVs contains active pore-forming listeriolysin (LLO), internalin B (inlB), phosphatidylinositol-specific phospholipase C (PI-PLC-A). We have previously reported that MVs of L. monocytogenes can infect and induce cytotoxicity in Caco-2 cells. In this study, we report the transcriptome response of Caco-2 cells upon infection with MVs as well as L. monocytogenes. In particular, we observed the up-regulation of autophagy-related genes in the early phase of infection with MVs. Transcription of inflammatory cytokines (CCL2, CXCL6, CXCL8, CXCL15, CXCL5, CXCL10) peaked at four h of infection. A large number of differentially expressed genes was associated with actin cytoskeleton rearrangement, autophagy, cell cycle arrest, and induction of oxidative stress. At a later time point, transcriptional programs generated upon infection with MVs point toward to evade innate immune signals, by modulating the expression of anti-inflammatory genes. KEGG pathway enrichment analysis revealed that MVs induce several signaling pathways such as PI3k-Akt signaling pathway, mitogen-activated protein kinase (MAPK) pathway, NOD-like receptor signaling pathway, cAMP signaling pathway, TNF, and NF-kB signaling pathway. Moreover, MVs induced the expression of cell cycle regulatory genes, which may result in the ability to prolong host cell survival, thus protecting the replicative niche for L. monocytogenes. Notably, we identified several non-coding RNAs (ncRNAs) are regulated during infection, suggesting that an early manipulation of the host gene expression may be essential for L. monocytogenes persistence and replication in host cells.

scholarly journals Effects of Fibronectin 1 on Cell Proliferation, Senescence and Apoptosis of Human Glioma Cells Through the PI3K/AKT Signaling Pathway

2018 ◽  
Vol 48 (3) ◽  
pp. 1382-1396 ◽  
Author(s):  
Yu-Xiang Liao ◽  
Zhi-Ping Zhang ◽  
Jie Zhao ◽  
Jing-Ping Liu
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Enrichment Analysis ◽  
Akt Signaling ◽  
Pathway Enrichment Analysis ◽  
Akt Signaling Pathway ◽  
Go Enrichment ◽  
Go Enrichment Analysis

Background/Aims: The current study aimed to investigate the role by which fibronectin 1 (FN1) influences the cell cycle, senescence and apoptosis in human glioma cells through the PI3K/ AKT signaling pathway. Methods: Differentially expressed genes (DEGs) were identified based on gene expression data (GSE12657, GSE15824 and GSE45921 datasets) and probe annotation files from Gene Expression Omnibus. The DEGs were identified in connection with gene ontology (GO) enrichment analysis and with the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. The positive expression of the FN1 protein was detected by immunohistochemistry. The glioma cell lines U251 and T98G were selected and assigned into blank, negative control (NC) and siRNA-FN1 groups. A dual luciferase reporter gene assay was used to investigate the effects of FN1 on transcriptional activity through the PI3K/AKT signaling pathway. An MTT assay was applied for the detection of cell proliferation, while flow cytometry was employed for cell cycle stage and cellular apoptosis detection. β-galactosidase staining was utilized to detect cellular senescence, a scratch test was applied to evaluate cell migration, and a transwell assay was used to analyze cell invasion. Western blotting and qRT-PCR methods were used to detect the protein and mRNA expression levels, respectively, of the FN1 gene and the related genes in the PI3K/AKT pathway (PI3K, AKT and PTEN), the cell cycle (pRb, CDK4 and Cyclin D1) and cell senescence (p16 and p21) among the collected tissues and cells. Results: GSE12657 profiling revealed FN1 to be the most upregulated gene in glioma. Regarding the GSE12657 and GSE15824 datasets, FN1 gene expression was higher in glioma tissues than in normal tissues. GO enrichment analysis and KEGG pathway enrichment analysis indicated that FN1 is involved in the synthesis of extracellular matrix (ECM) components and the PI3K/AKT signaling pathway. Verification was provided, indicating the role played by the FN1 gene in the regulation of the PI3K/AKT signaling pathway, as silencing the FN1 gene was found to inhibit cell proliferation, promote cell apoptosis and senescence, and reduce migration and invasion through the down-regulation of FN1 gene expression and disruption of the PI3K-AKT signaling pathway. Conclusion: The findings of this study provide evidence highlighting the prominent role played by FN1 in stimulating glioma growth, invasion, and survival through the activation of the PI3K/AKT signaling pathway.

scholarly journals ERK Is a Critical Regulator of JC Polyomavirus Infection

2018 ◽  
Vol 92 (7) ◽  
Author(s):  
Jeanne K. DuShane ◽  
Michael P. Wilczek ◽  
Colleen L. Mayberry ◽  
Melissa S. Maginnis
Keyword(s):  
Viral Infection ◽  
Signaling Pathway ◽  
Demyelinating Disease ◽  
Mapk Pathway ◽  
Host Cells ◽  
Mitogen Activated Protein Kinase ◽  
Jc Polyomavirus ◽  
Erk Activation ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

ABSTRACTThe human JC polyomavirus (JCPyV) infects the majority of the population worldwide and presents as an asymptomatic, persistent infection in the kidneys. In individuals who are immunocompromised, JCPyV can become reactivated and cause a lytic infection in the central nervous system resulting in the fatal, demyelinating disease progressive multifocal leukoencephalopathy (PML). Infection is initiated by interactions between the capsid protein viral protein 1 (VP1) and the α2,6-linked sialic acid on lactoseries tetrasaccharide c (LSTc), while JCPyV internalization is facilitated by 5-hydroxytryptamine 2 receptors (5-HT2Rs). The mechanisms by which the serotonin receptors mediate virus entry and the signaling cascades required to drive viral infection remain poorly understood. JCPyV was previously shown to induce phosphorylation of extracellular signal-regulated kinase (ERK), a downstream target of the mitogen-activated protein kinase (MAPK) pathway, upon virus entry. However, it remained unclear whether ERK activation was required for JCPyV infection. Both ERK-specific small interfering RNA (siRNA) and ERK inhibitor treatments resulted in significantly diminished JCPyV infection in both kidney and glial cells yet had no effect on the infectivity of the polyomavirus simian virus 40 (SV40). Experiments characterizing the role of ERK during steps in the viral life cycle indicate that ERK activation is required for viral transcription, as demonstrated by a significant reduction in production of large T antigen (TAg), a key viral protein associated with the initiation of viral transcription and viral replication. These findings delineate the role of the MAPK-ERK signaling pathway in JCPyV infection, elucidating how the virus reprograms the host cell to promote viral pathogenesis.IMPORTANCEViral infection is dependent upon host cell factors, including the activation of cellular signaling pathways. These interactions between viruses and host cells are necessary for infection and play an important role in viral disease outcomes. The focus of this study was to determine how the human JC polyomavirus (JCPyV), a virus that resides in the kidney of the majority of the population and can cause the fatal, demyelinating disease progressive multifocal leukoencephalopathy (PML) in the brains of immunosuppressed individuals, usurps a cellular signaling pathway to promote its own infectious life cycle. We demonstrated that the activation of extracellular signal-regulated kinase (ERK), a component of the mitogen-activated protein kinase (MAPK) pathway, promotes JCPyV transcription, which is required for viral infection. Our findings demonstrate that the MAPK-ERK signaling pathway is a key determinant of JCPyV infection, elucidating new information regarding the signal reprogramming of host cells by a pathogenic virus.

Systematic Investigation of Quercetin for Treating Cardiovascular Disease Based on Network Pharmacology

2019 ◽  
Vol 22 (6) ◽  
pp. 411-420 ◽  
Author(s):  
Xian-Jun Wu ◽  
Xin-Bin Zhou ◽  
Chen Chen ◽  
Wei Mao
Keyword(s):  
Cardiovascular Disease ◽  
Cardiovascular Diseases ◽  
Signaling Pathway ◽  
Kegg Pathway ◽  
Enrichment Analysis ◽  
Network Pharmacology ◽  
Pathway Enrichment Analysis ◽  
Therapeutic Effects ◽  
Pathway Enrichment ◽  
Compound Target

Aim and Objective: Cardiovascular disease is a serious threat to human health because of its high mortality and morbidity rates. At present, there is no effective treatment. In Southeast Asia, traditional Chinese medicine is widely used in the treatment of cardiovascular diseases. Quercetin is a flavonoid extract of Ginkgo biloba leaves. Basic experiments and clinical studies have shown that quercetin has a significant effect on the treatment of cardiovascular diseases. However, its precise mechanism is still unclear. Therefore, it is necessary to exploit the network pharmacological potential effects of quercetin on cardiovascular disease. Materials and Methods: In the present study, a novel network pharmacology strategy based on pharmacokinetic filtering, target fishing, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, compound-target-pathway network structured was performed to explore the anti- cardiovascular disease mechanism of quercetin. Results:: The outcomes showed that quercetin possesses favorable pharmacokinetic profiles, which have interactions with 47 cardiovascular disease-related targets and 12 KEGG signaling pathways to provide potential synergistic therapeutic effects. Following the construction of Compound-Target-Pathway (C-T-P) network, and the network topological feature calculation, we obtained top 10 core genes in this network which were AKT1, IL1B, TNF, IL6, JUN, CCL2, FOS, VEGFA, CXCL8, and ICAM1. KEGG pathway enrichment analysis. These indicated that quercetin produced the therapeutic effects against cardiovascular disease by systemically and holistically regulating many signaling pathways, including Fluid shear stress and atherosclerosis, AGE-RAGE signaling pathway in diabetic complications, TNF signaling pathway, MAPK signaling pathway, IL-17 signaling pathway and PI3K-Akt signaling pathway.

CENPF/CDK1 Signaling Pathway Enhances the Progression of Adrenocortical Carcinoma by Regulating the G2/M-phase Cell Cycle

2021 ◽  
Author(s):  
Yugang Huang ◽  
Dan Li ◽  
Li Wang ◽  
Xiaomin Su ◽  
Xian-bin Tang
Keyword(s):  
Cell Cycle ◽  
Signaling Pathway ◽  
Adrenocortical Carcinoma ◽  
Immune Cell ◽  
Interaction Network ◽  
Enrichment Analysis ◽  
Gene Set Enrichment Analysis ◽  
Phase Cell ◽  
Aberrant Expression ◽  
M Phase

Abstract Adrenocortical carcinoma (ACC) is an aggressive and rare malignant tumor and prone to local invasion and metastasis. While, overexpressed Centromere Protein F (CENPF) is closely related to oncogenesis of various neoplasms, including ACC. However, the prognosis and exact biological function of CENPF in ACC remains largely unclear. In present essay, the expression of CENPF in human ACC samples, GEO and TCGA databases depicted that CENPF were overtly hyper-expressed in ACC patients and positively correlated with tumor stage. The aberrant expression of CENPF was significantly correlated with unfavorable overall survival (OS) in ACC patients. Then, the application of gene-set enrichment analysis (GSEA) declared that CENPF was mainly involved in the G2/M-phase mediated cell cycle and p53 signaling pathway. Further, a small RNA interference experiment was conducted to demonstrate that the interaction between CENPF and CDK1 enhanced the G2/M-phase transition of mitosis, cell proliferation and might induce p53 mediated anti-tumor effect in human ACC cell line, SW13 cells. Lastly, two available therapeutic strategies, including immunotherapy and chemotherapy, have been further probed. Immune infiltration analysis highlighted that ACC patients with high CENPF expression harbored significantly different immune cell populations, and high TMB/MSI score. Then, the gene-drug interaction network stated that CENPF inhibitors, such as Cisplatin, Sunitinib, and Etoposide, might serve as potential drugs for the therapy of ACC. Briefly, CENPF and related genes might be served as a novel prognostic biomarker or latent therapeutic target for ACC patients.

scholarly journals MicroRNA expression profiling involved in Borax-induced anti-tumor effect using gene-chip analysis

2020 ◽  
Author(s):  
Lun Wu ◽  
Ying Wei ◽  
Wen-Bo Zhou ◽  
Jiao Zhou ◽  
Li-Hua Yang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Hepg2 Cells ◽  
Enrichment Analysis ◽  
Gene Chip ◽  
Differentially Expressed ◽  
Control Group ◽  
Pathway Enrichment Analysis ◽  
Ras Signaling ◽  
Therapeutic Benefits ◽  
Differentially Expressed Mirnas

Abstract Background Borax, a boron compound, which is becoming widely recognized for its biological effects, including antioxidant activity, cytotoxicity, and potential therapeutic benefits. However, the specific molecular mechanisms underlying borax-induced anti-tumor effect still remain to be to further elucidated. MicroRNAs (miRNAs) may play key roles in cellular processes including tumor progression, cell apoptosis and cytotoxicity. Thus, this study aimed to investigate, whether miRNAs were involved in the borax-mediated anti-tumor effect using miRNA profiling of a human liver cancer cell line (HepG2) using gene-chip analysis.Methods Total RNA was extracted and purified from HepG2 cells that were treated with 4 mM borax for either 2 or 24 h. The samples underwent microarray analysis using an Agilent Human miRNA Array. Differentially expressed miRNAs were analysed by volcano plot and heatmap, and were validated using real-time fluorescent quantitative PCR (qPCR).ResultsAmong this, 2- or 24-h exposure to borax significantly altered the expression level of miRNAs in HepG2 cells, 4 or 14 were upregulated and 3 were downregulated compared with the control group, respectively (≥2-fold; P<0.05). GO enrichment analysis and KEGG pathway enrichment analysis revealed that target genes of differentially expressed miRNAs in HepG2 cells predominantly participated in MAPK signaling pathway, TGF-beta signaling pathway, NF-kappa B signaling pathway, etc; in 2-h borax treatment group, while Ras signaling pathway, FoxO signaling pathway, Cellular senescence, etc; involved in 24-h treatment group.Conclusions Result indicates that borax-induced anti-tumor effect may be associated with alterations in miRNAs.

scholarly journals The Mechanism Study of Xiao-Xian-Xiong Decoction in the Treatment of Atherosclerosis with Network Pharmacology

2020 ◽  
Author(s):  
Liucheng Xiao ◽  
Zonghuan Li ◽  
Chongyuan Fan ◽  
Chenggong Zhu ◽  
Xingyu Ma ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Mapk Pathway ◽  
Enrichment Analysis ◽  
Foam Cells ◽  
Functional Enrichment ◽  
Network Pharmacology ◽  
Mechanism Study ◽  
Ppi Networks

Abstract Background: Xiao-Xian-Xiong decoction is a useful formula in the treatment of atherosclerosis in traditional Chinese medicine. In this study, we aimed to investigate the function of Xiao-Xian-Xiong decoction in the treatment of atherosclerosis. Methods: In this study, we conducted the method of network pharmacology and molecular docking to discover the mechanism of Xiao-Xian-Xiong decoction against atherosclerosis. Then, we validated the function of Xiao-Xian-Xiong decoction in atherosclerosis in vitro. We investigated the function and mechanism of Xiao-Xian-Xiong decoction in RAW264.7 macrophage-derived foam cells.Results: We identified 213 targets of Xiao-Xian-Xiong decoction and 331 targets of atherosclerosis. The PPI networks of Xiao-Xian-Xiong decoction and atherosclerosis were constructed. Furthermore, the two PPI networks were merged and the core PPI network was obtained. Then, functional enrichment analysis was conducted with GO and KEGG signaling pathway analysis. KEGG analysis indicated Xiao-Xian-Xiong decoction was correlated with ubiquitin mediated proteolysis pathway, PI3K-AKT pathway, MAPK pathway, Notch signaling pathway, and TGF-β signaling pathway. At last, we validated the function of Xiao-Xian-Xiong decoction with atherosclerosis in vitro. Xiao-Xian-Xiong decoction reduced lipid accumulation and promoted the outflow of cholesterol in RAW264.7-derived foam cells. Xiao-Xian-Xiong decoction increased the expression of ABCA1 and ABCG1 protein in foam cells. ABCA1 and ABCG1 were related with regulation of the inflammatory pathway and cell proliferation in atherosclerosis.Conclusions: Combined the mechanism of available treatments of atherosclerosis, we inferred Xiao-Xian-Xiong decoction could alleviate atherosclerosis by inhibiting inflammatory response and cell proliferation.

scholarly journals Comprehensive Analysis of the Immune and Prognostic Implication of MMP14 in Lung Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-21
Author(s):  
Chun-long Zheng ◽  
Qiang Lu ◽  
Nian Zhang ◽  
Peng-yu Jing ◽  
Ji-peng Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Signaling Pathway ◽  
Lung Squamous Cell Carcinoma ◽  
Enrichment Analysis ◽  
Cell Receptor ◽  
Risk Scores ◽  
Pathway Enrichment Analysis ◽  
Receptor Signaling ◽  
Immune Infiltration ◽  
Receptor Signaling Pathway

More and more studies have indicated an association between immune infiltration in lung cancer and clinical outcomes. Matrix metalloproteinase 14 (MMP14) has been reported to be dysregulated in many types of tumors and involved in the development and progression of tumors. However, its contribution to cancer immunity was rarely reported. In the study, we found that MMP14 expression was distinctly upregulated in lung cancer specimens compared with nontumor lung specimens. High MMP14 expression predicted a poor prognosis of lung squamous cell carcinoma (LUSC) patients. Increased MMP14 expressions were observed to be positively related to high immune infiltration levels in most of the immune cells. A pathway enrichment analysis of 32 MMP14-associated immunomodulators indicated the involvement of T cell receptor signaling pathway and Toll-like receptor signaling pathway. Based on MMP14-associated immunomodulators, we applied multivariate assays to construct multiple-gene risk prediction signatures. We observed that risk scores were independently associated with overall survival. These data highlighted that MMP14 was involved in tumor immunity, indicating that MMP14 could serve as a novel prognostic biomarker and therapeutic target for lung cancer. Our data suggest that the four genes identified in this study may serve as valuable biomarkers of lung cancer patient outcomes.

MAPK: A promising signaling pathway in targeted therapy for the treatment of NSCLC

2021 ◽  
Vol 16 (7) ◽  
pp. 231-239
Author(s):  
Muthu Kumar Thirunavukkarasu ◽  
Ramanathan Karuppasamy
Keyword(s):  
Lung Cancer ◽  
Signaling Pathway ◽  
Checkpoint Inhibitors ◽  
Mapk Pathway ◽  
Nonsmall Cell Lung Cancer ◽  
Mitogen Activated Protein Kinase ◽  
Oncogenic Mutations ◽  
Mitogen Activated Protein ◽  
Protein Kinase Signaling ◽  
Kinase Signaling Pathway

Aberrant stimulation of MAPK (Mitogen-activated protein kinase) signaling pathway triggers the dysregulated cell growth and resistance to apoptosis in a wide variety of tumors especially in NSCLC (Nonsmall cell lung cancer). Most of the research is on treating lung cancer by targeting the MAPK pathway receptors. Nevertheless, it is essential to consider interconnections and mode of action to resolve the drug resistance ad feedback loops during the treatment with checkpoint inhibitors. Here we describe the overall mechanism of MAPK pathway, oncogenic mutations and precise information regarding the drug compounds for each receptor in this pathway. Further, in-depth insights into this review could be beneficial for the empathetic discovery of inhibitors for NSCLC against this pathway.

scholarly journals Integrating Network Pharmacology with Molecular Docking to Unravel the Active Compounds and Potential Mechanism of Simiao Pill Treating Rheumatoid Arthritis

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Mengshi Tang ◽  
Xi Xie ◽  
Pengji Yi ◽  
Jin Kang ◽  
Jiafen Liao ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Molecular Docking ◽  
Signaling Pathway ◽  
Target Genes ◽  
Enrichment Analysis ◽  
Binding Activity ◽  
New Combination ◽  
Network Pharmacology ◽  
Pathway Enrichment Analysis ◽  
Potential Mechanism

Objective. To explore the main components and unravel the potential mechanism of simiao pill (SM) on rheumatoid arthritis (RA) based on network pharmacological analysis and molecular docking. Methods. Related compounds were obtained from TCMSP and BATMAN-TCM database. Oral bioavailability and drug-likeness were then screened by using absorption, distribution, metabolism, and excretion (ADME) criteria. Additionally, target genes related to RA were acquired from GeneCards and OMIM database. Correlations about SM-RA, compounds-targets, and pathways-targets-compounds were visualized through Cytoscape 3.7.1. The protein-protein interaction (PPI) network was constructed by STRING. Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed via R packages. Molecular docking analysis was constructed by the Molecular Operating Environment (MOE). Results. A total of 72 potential compounds and 77 associated targets of SM were identified. The compounds-targets network analysis indicated that the 6 compounds, including quercetin, kaempferol, baicalein, wogonin, beta-sitosterol, and eugenol, were linked to ≥10 target genes, and the 10 target genes (PTGS1, ESR1, AR, PGR, CHRM3, PPARG, CHRM2, BCL2, CASP3, and RELA) were core target genes in the network. Enrichment analysis indicated that PI3K-Akt, TNF, and IL-17 signaling pathway may be a critical signaling pathway in the network pharmacology. Molecular docking showed that quercetin, kaempferol, baicalein, and wogonin have good binding activity with IL6, VEGFA, EGFR, and NFKBIA targets. Conclusion. The integrative investigation based on bioinformatics/network topology strategy may elaborate on the multicomponent synergy mechanisms of SM against RA and provide the way out to develop new combination medicines for RA.

scholarly journals A System-Level Investigation into the Mechanisms of Apigenin Against Inflammation

2019 ◽  
Vol 14 (9) ◽  
pp. 1934578X1987860 ◽  
Author(s):  
Ying Xie ◽  
Dongdong Liang ◽  
Qingke Wu ◽  
Xuemei Chen ◽  
Manal Ali Buabeid ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Biological Activities ◽  
Enrichment Analysis ◽  
Underlying Mechanism ◽  
Mitogen Activated Protein Kinase ◽  
System Level ◽  
Network Pharmacology ◽  
Pathway Enrichment Analysis ◽  
Biological Processes ◽  
Go Terms

Apigenin is a natural flavone that possesses excellent biological activities especially against aging and cancer. However, the underlying mode of its action is not yet revealed. The purpose of this study was to examine the pharmacological mechanisms of apigenin using the knowledge of network pharmacology, protein-protein interaction (PPI) databases and biological processes analysis through Cytoscape. Apigenin targets were retrieved through PASS Prediction and STITCH database and the interactive associations between these targets were studied using STITCH, followed by GO (gene ontology) and pathway enrichment analysis. As a result of target search, 125 protein targets were retrieved. Moreover, 216 GO terms related to various biological processes, 16 GO terms for various molecular processes, 5 GO terms for the cellular components, and 52 Kyoto Encyclopedia of Genes and Genomes pathway terms were achieved by analyzing gene functional annotation clusters and abundance values of these targets. Most of these terms are strongly associated with inflammation through various pathways, for example, FOXO, mammalian target of rapamycin, tumor necrosis factor, p53, AMP-activated protein kinase, p13K-AKT, and mitogen-activated protein kinase, which play an important role in inflammation, aging and cancer. Apigenin can be used to treat inflammation, aging, and cancer with an underlying mechanism of inflammation suppression. This study contributed excellent information for a better understanding of the modes of action of apigenin. However, further studies such as docking and MD simulation are required to understand the therapeutic and toxicological roles of these targets of apigenin.

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