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ScGOclust: leveraging gene ontology to find functionally analogous cell types between distant species.

MOTIVATION: Basic biological processes are shared across animal species, yet their cellular mechanisms are profoundly diverse. Comparing cell-type gene expression between species reveals conserved and divergent cellular functions. However, as phylogenetic distance increases, gene-based comparisons become less informative. The gene ontology (GO) knowledgebase offers a solution by serving as the most comprehensive resource of gene functions across a vast diversity of species, providing a bridge for distant species comparisons. RESULTS: Here, we present scGOclust, a computational tool that constructs de novo cellular functional profiles using GO terms, facilitating systematic and robust comparisons within and across species. We applied scGOclust to analyse and compare the heart, gut, and kidney between mouse and fly, and whole-body data from Caenorhabditis elegans and Hydra vulgaris. We show that scGOclust effectively recapitulates the function spectrum of different cell types, characterizes functional similarities between homologous cell types, and reveals functional convergence between unrelated cell types. Additionally, we identified subpopulations within the fly crop that show circadian rhythm-regulated secretory properties and hypothesize an analogy between fly principal cells from different segments and distinct mouse kidney tubules. We envision scGOclust as an effective tool for uncovering functionally analogous cell types or organs across distant species, offering fresh perspectives on evolutionary and functional biology. AVAILABILITY AND IMPLEMENTATION: ScGOclust is publicly available on CRAN: https://cran.r-project.org/web/packages/scGOclust/index.html and development versions are available on GitHub: github.com/Papatheodorou-Group/scGOclust/.

Animals

Identification of key genes related to bone metastasis of breast cancer using bioinformatics methods and construction of a prognostic model.

Breast cancer (BC) ranks among the most prevalent cancers in females, with bone metastasis significantly compromising patients' quality of life and survival rates. Enhancing our comprehension of BC bone metastasis mechanisms at the molecular level holds promise for improving BC treatment and prognosis. Leveraging bioinformatics tools, we integrated multiple datasets, conducted comprehensive analyses across various databases, identified biomarkers associated with BC bone metastasis, and constructed a prognostic model. Firstly, 3 BC bone metastasis-related datasets were downloaded from gene expression omnibus, the data were merged, and batch effects were removed, followed by identification of differentially expressed genes (DEGs). Gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on the DEGs. A protein-protein interaction network was constructed using the STRING database to screen hub genes. Then, survival analysis of hub genes was performed using the Cancer Genome Atlas (TCGA) database. A prognostic model was constructed using key genes with survival differences, and the model was evaluated. Two hundred ninety-two DEGs were identified. Gene ontology and KEGG pathway enrichment analysis yielded 769 biological processes (BPs), 78 cellular components, 43 molecular functions, and 50 KEGG pathways. Fifteen hub genes were selected from the protein-protein interaction network. Survival analysis revealed 6 genes related to BC survival. The prognostic model identified 4 genes with important predictive value for BC prognosis. Our study utilized bioinformatics analysis to identify a series of DEGs related to BC bone metastasis. Based on further selection of hub genes, we constructed a relatively ideal prognostic model for BC, and identified 4 genes (DLGAP5, TPX2, PLK1, and CENPN) with valuable predictive value for BC prognosis.

Humans

Molecular mechanism of HaiZao-YuHu decoction in breast cancer treatment via network pharmacology and molecular docking: Computational pharmacology.

BACKGROUND: The molecular biological mechanisms of HaiZao-YuHu decoction were investigated using network pharmacology and molecular docking. METHODS: TCMSP database was used to collect the active ingredients and action targets of HaiZao-YuHu decoction, through the OMIM, PharmGkb, GeneCards, TDD, and DurgBank database query targets for breast cancer. Then, using the intersecting targets, the protein-protein interaction network of HaiZao-YuHu decoction was constructed using the STRING website. Network topology analysis was performed using Cytoscape 3.9.0 to identify the core targets. Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed with the R package. The Autodock software was used for molecular docking. RESULTS: Thirty-four active ingredients, 219 intersection targets and 4 key targets were obtained. gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analysis get 2152 biological processes and 186 pathways. Molecular docking showed that the 4 core targets could combine well with the 5 main active components. CONCLUSION: HaiZao-YuHu decoction can play a role in the treatment of breast cancer through multi-targets, multi-components, and multi-pathways.

Molecular Docking Simulation

Analysis of the molecular mechanism underlying di(2-ethylhexyl) phthalate-induced bladder carcinogenesis via network toxicology and molecular docking approaches: An observational study.

This study aims to investigate the toxicity of di(2-ethylhexyl) phthalate (DEHP) and the potential molecular mechanisms of DEHP-induced bladder cancer (BLCA) using network toxicology and molecular docking strategies. The toxicity of DEHP was assessed using Prox-II software, and potential targets for DEHP-induced BLCA were identified by integrating data from ChEMBL database, Search Tool for Interactions of Chemicals, SwissTargetPrediction, GeneCards, Therapeutic Target Database, Online Mendelian Inheritance in Man, and The Cancer Genome Atlas. STRING database and Cytoscape were employed to construct target networks and determine core targets. The expression levels of core targets were analyzed using R. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed on potential and core targets. Molecular docking was carried out using CB-Dock 2 to verify the interactions between DEHP and core targets. A total of 105 potential targets related to DEHP-induced BLCA were identified, from which 7 core targets were selected: cyclin-dependent kinase 1, interleukin 6, cyclin-dependent kinase 2, cyclin B1, Erb-B2 receptor tyrosine kinase 2, cyclin B2, and B-cell lymphoma 2. IL-6 and B-cell lymphoma 2 showed downregulated expression in tumor tissues, while cyclin-dependent kinase 1, cyclin-dependent kinase 2, cyclin B1, Erb-B2 receptor tyrosine kinase 2, and cyclin B2 were upregulated. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses indicated that these targets were enriched in cell signaling and cancer-related pathways. Molecular docking confirmed that DEHP interacts with these core targets. DEHP may promote the development of BLCA by interacting with key proteins and signaling pathways. This study provides a theoretical basis for understanding the molecular mechanisms of DEHP-induced BLCA and offers references for future prevention and treatment strategies.

Diethylhexyl Phthalate

Unique signatures of highly constrained genes across publicly available genomic databases.

PURPOSE: Publicly available genomic databases are critical in understanding human genetic variation. They also provide unique insights into patterns of genetic constraints and their relationship with human disease. METHODS: We utilized one of the largest publicly available databases, Genome Aggregate Database, to determine genes that are highly constrained for only loss-of-function, only missense, and both loss-of-function/missense variants. We identified their unique signatures and explored their causal relationship with human diseases. Those genes were also evaluated for chromosomal location, tissue-level expression, Gene Ontology analysis, and gene family categorization using multiple publicly available databases. RESULTS: We identified unique patterns of inheritance, protein size, and enrichment in distinct molecular pathways for those constrained genes associated with human disease. In addition, we identified genes that are currently not known to cause human disease, which may be excellent gene discovery candidates. CONCLUSION: We elucidate biological pathways of highly constrained genes that expand our understanding of critical cellular proteins. The findings can also advance research in rare diseases.

Humans

Exploring prognostic genes in the immune microenvironment of acute myeloid leukemia via weighted gene co-expression network analysis.

BACKGROUND: Acute myeloid leukemia (AML) is a heterogeneous blood cancer that arises from transformed myeloid precursor cells in a compromised bone marrow microenvironment. This environment is essential for AML initiation, progression, and relapse. Alongside oncogenic changes in hematopoietic cells, immunological dysregulation also contributes to leukemogenesis. The present study is aimed to identify prognostic genes in stromal and immune cells associated with AML using the weighted gene co-expression network analysis (WGCNA). METHODS: Gene expression profiles were retrieved from The Cancer Genome Atlas database, and immune and stromal cell scores were calculated using the ESTIMATE (Estimation of STromal and Immune cells in MAlignant Tumor tissues using Expression data) method. These scores helped identify differentially expressed genes (DEGs), which were then used to create gene clusters through WGCNA. To explore the functions of genes linked to AML subtypes, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed. A protein-protein interaction network was developed to identify hub genes. The top 18 hub genes were identified using the cytoHubba plug-in in Cytoscape software, and survival analysis was conducted with the Gene Expression Profiling Interactive Analysis 2 online tool. RESULTS: A total of 1097 DEGs were identified, with 601 being upregulated and 496 downregulated. WGCNA analysis indicated that the gray module, comprising 165 genes, had the strongest association with AML subtypes (Cor&#x2005;>&#x2005;0.3; P&#x2005;<&#x2005;.05). Gene Ontology enrichment analysis demonstrated that the 18 identified hub genes were predominantly associated with neutrophil activation, immune response, secretory granule membrane, and pattern recognition receptor activity. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis revealed that the DEGs were mainly involved in pathways related to phagosome, lysosome, tuberculosis, leishmaniasis, and neutrophil extracellular trap formation. Kaplan-Meier survival analysis of the top 18 hub genes indicated that ITGAM, IL10, and CD163 were significantly correlated with survival outcomes in AML. CONCLUSION: Key stromal and immune-related genes influencing AML patient outcomes were identified, highlighting their potential as therapeutic targets. These discoveries provide deeper insights into the molecular mechanisms driving AML pathogenesis and subtype differentiation.

Leukemia, Myeloid, Acute

Comprehensive Analysis of Differentially Expressed Genes and Immune Infiltration in Burn Injury: Key Biomarkers and Pathways.

BACKGROUND: Burn injuries trigger complex immune responses and gene expression changes, impacting wound healing and systemic inflammation. Understanding these changes is crucial for identifying biomarkers and therapeutic targets. METHODS: We analyzed two gene expression omnibus datasets (wound tissue [GSE8056] and blood [GSE37069]) to identify differentially expressed genes (DEGs) in burn injury samples versus controls. Immune cell proportions were assessed using CIBERSORT. Functional enrichment analyses (Gene Ontology and Kyoto Encyclopedia of Genes and Genomes) and protein-protein interaction networks were constructed to identify key genes and pathways. RESULTS: We identified 1170 upregulated and 1227 downregulated DEGs. Gene Ontology analysis revealed enrichment in neutrophil activation, inflammatory response, and extracellular matrix organization. Kyoto Encyclopedia of Genes and Genomes analysis highlighted cytokine-cytokine receptor interaction, TNF, and IL-17 signaling pathways. Immune infiltration analysis showed significant changes in neutrophils, macrophages (M1/M2), and T-cell subsets. Protein-protein interaction network analysis identified five hub genes: JUN, STAT1, Bcl2, MMP9, and TLR2. CONCLUSIONS: This study provides a comprehensive bioinformatic analysis of gene expression and immune responses in burn injuries. The identified DEGs, hub genes, and pathways offer insights into the immune response mechanisms and suggest potential targets for diagnostic and therapeutic interventions in burn injury management.

Burns

In silico analysis based on network pharmacology and biomolecular informatics to explore the mechanism of action of Erjing Pills (from Shengji Zonglu) in the treatment of leukotrichia.

This study aimed to explore the core active ingredients and potential molecular mechanisms of Erjing Pills, a prescription in the classic work of Traditional Chinese Medicine, "Shengji Zonglu," in the treatment of leukotrichia by utilizing network pharmacology and biomolecular docking techniques. The chemical components and potential targets of Chinese herbal medicines were analyzed through databases such as the Traditional Chinese Medicine Systems Pharmacology Database. The targets related to leukotrichia were collected using GeneCards. The intersection targets were obtained using RStudio. The protein-protein interaction (PPI) network map and the "drug-component-target-disease" visualization network were generated using Cytoscape and STRING to screen the core components and key targets. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were carried out using the Database for Annotation, Visualization and Integrated Discovery and RStudio. Finally, molecular docking verification was performed by AutoDock and PyMOL (Schr&#xf6;dinger LLC). The key active ingredients of Erjing Pills in the treatment of leukotrichia are &#x3b2;-sitosterol, quercetin, baicalein, and stigmasterol. The top 5 PPI core target proteins, in order, are AKT serine/threonine kinase 1, interleukin 6, tumor protein p53, cysteine-aspartic acid protease 3, and interleukin 1 beta. The Gene Ontology enrichment analysis suggests that the biological processes mainly include responses to exogenous stimuli, membrane rafts, and DNA-binding transcription factor binding. The Kyoto Encyclopedia of Genes and Genomes pathways involve signal pathways such as lipid and atherosclerosis, hepatitis B, Kaposi sarcoma virus infection, chemical carcinogenesis, and human cytomegalovirus infection. The molecular docking results indicate that most of the main active ingredients in Erjing Pills have relatively stable binding activities with the key targets, such as AKT serine/threonine kinase 1, interleukin 6, tumor protein p53, cysteine-aspartic acid protease 3, and interleukin 1 beta, in the PPI network. The active ingredients of Erjing Pills may interfere with the pathological process of leukotrichia by regulating key targets and signal pathways. This study provides a theoretical basis for the clinical application of Erjing Pills and indicates the direction for subsequent experimental research.

Drugs, Chinese Herbal

Investigating the molecular mechanism of Yangxin decoction in treating major depressive disorder using network pharmacology and molecular docking technology approaches.

Yangxin decoction has been used to treat major depressive disorder (MDD). This study aims to identify the active components and potential mechanisms of Yangxin decoction in treating MDD using network pharmacology and molecular docking technology. The active components and targets of Yangxin decoction were screened, and MDD-related targets were predicted. Networks of "herbal medicine-active components-potential targets" and protein-protein interaction were constructed. Core components and core targets were identified through network topology analysis. Gene ontology functional and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed on candidate genes. Molecular docking was conducted using AutoDock software (Olson Laboratory of the Scripps Research Institute, San Diego) to explore the interactions between core targets and active components, and the results were visualized using PyMOL (DeLano Scientific LLC, South San Francisco). A total of 433 active components and 392 targets of Yangxin decoction were identified, along with 11,796 MDD-related targets. There were 680 overlapping targets between Yangxin decoction and MDD, associated with 104 active components. Core targets identified through network topology analysis and molecular docking included serine/threonine kinase 1 (AKT1), tumor necrosis factor, interleukin-6, tumor protein P53, and proto-oncogene tyrosine-protein kinase Src. Gene ontology enrichment analysis revealed 1606 biological processes, 191 cellular components, and 373 molecular functions. Kyoto Encyclopedia of Genes and Genomes pathway analysis identified 212 signaling pathways, with significant enrichment in caffeine metabolism, bladder cancer, advanced glycation end products-receptor for advanced glycation end products signaling pathway in diabetic complications, and vascular endothelial growth factor signaling pathway. Molecular docking results showed strong binding energy between core active components and core targets. Yangxin decoction exhibits multi-component, multi-pathway, and multi-target therapeutic characteristics. It primarily regulates targets such as AKT1, tumor necrosis factor, interleukin-6, tumor protein P53, and proto-oncogene tyrosine-protein kinase Src through advanced glycation end products-receptor for advanced glycation end products, vascular endothelial growth factor, and ErbB signaling pathways, exerting anti-inflammatory, immune-regulating, and oxidative stress-inhibiting effects to alleviate MDD.

Molecular Docking Simulation

Identification of mitophagy-related biomarkers with immune cell infiltration in psoriasis.

BACKGROUND: Psoriasis is an inflammatory disorder characterized by scaly erythematous plaques and significant comorbidities. Recent studies have suggested that impaired mitophagy, the cellular mechanism for removing dysfunctional mitochondria, may contribute to the pathogenesis of psoriasis. METHODS: In this study, we analyzed bulk RNA sequencing data from 167 healthy individuals and 177 patients with psoriasis obtained from the Gene Expression Omnibus database (GSE30999 and GSE54456). Mitophagy-related genes were isolated using weighted gene co-expression network analysis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed and protein-protein interaction networks were constructed for the functional enrichment of genes associated with mitophagy. The correlations between genes associated with mitophagy, signaling pathways, and immune cell infiltration were analyzed. The potential diagnostic value of genes associated with mitophagy was evaluated using receiver operating characteristic (ROC) curves, which were validated in imiquimod-induced psoriatic skin lesions in mice. RESULTS: We identified 3,839 differentially expressed genes between healthy individuals and patients with psoriasis, and 23 genes were selected as hub genes showing a high correlation with mitophagy in psoriasis. GO and KEGG analyses revealed that hub and associated genes were significantly correlated with skin functions, such as epidermal development and keratinocyte differentiation. In addition, mitophagy-related genes were negatively associated with pro-inflammatory and pro-proliferation pathways in psoriasis. Among the immune cells, CD4+ T cells were most significantly affected by mitophagy-related genes. ROC analysis demonstrated that mitophagy-related genes, especially ACER1, C1ORF68, CST6, FLG2, GJB3, GJB5, GPRIN2, KRT2, and SPRR4 were potential biomarkers of psoriasis for use in diagnosis or treatment. CONCLUSIONS: Mitophagy-related genes play crucial roles in psoriasis and have potential use as biomarkers, providing insights into disease mechanisms and therapeutic targets. Further research may lead to the development of new strategies for psoriasis management.

Psoriasis

Identification and validation of the important role of KIF11 in the development and progression of endometrial cancer.

BACKGROUND: Human kinesin family member 11 (KIF11) plays a vital role in regulating the cell cycle and is implicated in the tumorigenesis and progression of various cancers, but its role in endometrial cancer (EC) is still unclear. Our current research explored the prognostic value, biological function and targeting strategy of KIF11 in EC through approaches including bioinformatics, machine learning and experimental studies. METHODS: The GSE17025 dataset from the GEO database was analyzed via the limma package to identify differentially expressed genes (DEGs) in EC. Functional enrichment analysis of the DEGs was conducted using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. DEGs were further screened for hub genes through protein-protein interaction (PPI) network analysis and machine learning. The role of the hub gene KIF11 in EC was analyzed using clinical data from the TCGA database. The expression of KIF11 in EC was subsequently validated in clinical samples. In vitro experiments were utilized to evaluate the effects of KIF11 on biological functions such as proliferation, migration, apoptosis, and the cell cycle in endometrial cancer cells. RESULTS: A total of 877 DEGs, which are widely involved in important biological processes such as cell division, tubulin binding, and the cell cycle, were identified. Through PPI network analysis and machine learning, KIF11 was selected as the hub gene for subsequent analysis and experimental validation. An analysis of TCGA data revealed that KIF11 is highly expressed in EC and is associated with tumor grade, stage, and a low survival rate. The overexpression of KIF11 in tumor tissues was further confirmed in EC patient samples. KIF11 knockdown had inhibitory effects on cell proliferation, migration and invasion. Flow cytometry analysis revealed that KIF11 knockdown induced G2/M phase arrest and promoted apoptosis in EC cells. CONCLUSION: Our study demonstrated that KIF11 was upregulated in EC and was strongly associated with a poor prognosis. Notably, we found that reduced KIF11 expression inhibited EC cell proliferation, migration and invasion. KIF11 knockdown caused more EC cells to arrest in the G2/M phase and undergo apoptosis. The findings of our study emphasized that KIF11 may be a promising prognostic biomarker and therapeutic target for EC patients.

Humans

Genes near tRNAs are enriched in translational machinery.

Transfer RNAs (tRNAs) are known for delivering amino acids to the growing polypeptide chain during translation. They can also influence gene expression, especially in times of nutrient starvation, through differential tRNA expression and modification. Transfer RNAs have a highly consistent cloverleaf structure, but relatively few known regulatory elements govern this conserved structure despite the 20 different standard isotypes. This study examines gene enrichment patterns near tRNA genes across 1149 fungal genomes. Genes enriched in proteasome regulation, ion transport, and rRNA were found to be significantly closer to tRNAs than other pathways. These results were consistent across KEGG overrepresentation analysis (ORA), KEGG gene set enrichment analysis (GSEA), and gene ontology (GO) analysis. Proteasome, ion transport, and RNA are all important aspects of protein production and regulation, suggesting that genes required for the synthesis and quality control of proteins, including tRNAs, are located near each other. Protein regulation is an energetically expensive process, and local co-regulation could increase efficiency and stress impacts on proteins.

RNA, Transfer

Proteomic hub proteins CDKN2B, TRAPPC2L, WFS1, and ARPP19 drive biochemical recurrence and metastatic progression in prostate cancer: Protein macromolecule action.

The biological characteristics and metastasis mechanism of prostate cancer are complex, involving the important role of many proteins in cell transcriptional regulation. This study focused on the role of the proteomic hub proteins CDKN2B, TRAPPC2L, WFS1 and ARPP19 in the biochemical recurrence and metastasis progression of prostate cancer. Cross-platform transcriptome integration and differential expression analysis were used to evaluate transcriptome characteristics in a prostate cancer cohort. Functional enrichment analysis was performed by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway annotation, and weighted gene co-expression network analysis (WGCNA) was used to investigate cancer progression subtypes. It was found that prostate cancer progression showed significant transcriptome heterogeneity, and low-expression genes dominated. We reveal the important role of epithelial-immune interactions and inflammatory signaling in transcriptional remodeling in prostate cancer. The co-expression network topology analysis showed that the immune-metabolic center module plays a central role in cancer progression. CDKN2B was identified as a key transcriptional determinant in prostate cancer typing, while TRAPPC2L and WFS1 acted as core transcriptional regulators, driving metastatic heterogeneity. ARPP19 and LOC650152 also show important transcriptional driving effects in advanced prostate cancer.

Humans

DNA methylome responses to biotic and abiotic stress in Arabidopsis thaliana: A multi-study analysis.

RATIONALE: Plants experience diverse biotic and abiotic stresses that can induce changes in DNA methylation. However, comparisons among existing studies are complicated by differences in analytical methods and experimental designs. We aimed to identify shared and stress-specific DNA methylation responses across studies. METHODS: We reanalysed 16 whole-genome bisulphite sequencing datasets from 13 Arabidopsis thaliana studies using a unified bioinformatics pipeline. Differentially methylated regions (DMRs) were assessed in the CG, CHG and CHH contexts and examined in relation to genes, transposable elements (TEs), Gene Ontology terms, gene-proximal TE superfamilies and epimutation-prone loci. RESULTS: Global methylation levels were generally stable, whereas the number and genomic distribution of DMRs varied according to stress type and methylation context. CG-DMRs occurred primarily in gene bodies, while CHG- and CHH-DMRs were enriched in TEs. Functional analysis identified shared stress-related processes across conditions. Gene-proximal LINE/L1, RathE1_cons and DNA/HAT elements were enriched for stress-responsive methylation changes. A subset of stress-associated CG-DMRs overlapped loci known to accumulate stable epimutations over generations. CONCLUSIONS: Standardized cross-study analysis revealed both shared and stress-specific methylation patterns. The association of stress-responsive DMRs with gene-proximal TEs and epimutation-prone loci suggests potential links among environmental responses, genome regulation and long-term epigenetic variation.

Arabidopsis thaliana

Bioinformatics identification and validation of pyroptosis-related gene for ischemic stroke.

BACKGROUND: Ischemic stroke (IS) is one of the common and frequent diseases with extremely high lethality and disability in the world, and there is no effective treatment at present. This study aimed to screen hub genes involved in cerebral ischemia/reperfusion injury (CIRI) and pyroptosis, and explore promising intervention targets. METHODS: CIRI-related genes (GSE202659 and GSE131193) and pyroptosis-related genes (PRGs) in mice were obtained from the Gene Expression Omnibus (GEO) and GeneCards database. We screened for LASSO regression to construct a prognostic model of GSE131193 and PRGs and examined by GSE137482. The functional enrichment analysis of Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene Set Enrichment Analysis (GSEA) and Gene Set Variation Analysis (GSVA) were performed on pyroptosis-related differentially expressed genes (PRDEGs) of GSE202659.The key modules for CIRI and pyroptosis were identified by Weight Gene Co-expression Network Analysis (WGCNA). Subsequently, Protein-protein Interaction (PPI) network and the Cytoscape was constructed to screen out hub genes. Used the starBase to predict miRNA interacting with hub genes and constructed mRNA-miRNA-lncRNA interaction networks. CIRI-related Molecular Subtypes were constructed for hub genes. The relationship between immune cells and hub genes was verified via CIBERSORT. Finally, we selected C57BL/6 mice to construct models to confirm hub genes by enzyme linked immunosorbent assay (ELISA), reverse transcription-polymerase chain reaction (RT-PCR), western blot, and Immunofluorescence. RESULTS: A total of 272 PRGs and 35 PRDEGs were screened. An eight-gene risk prediction models were established (AUC&#x2009;=&#x2009;0.868). GO, KEGG, GSEA and GSVA analyses revealed that PRDEGs were mainly involved in positive regulation of cytokine production, and NOD-like receptor signaling pathway. And then, seven hub genes (Irf1, Icam1, Tlr2, Tnf, Cebpb, Il1rn, and Casp8) were identified by PPI. Icam1, Tnf, Cebpb, Il1rn, and Casp8 had high expression profiles in Cluster2 by hierarchical clustering. The immune infiltration analysis results showed that among the hub genes, Cebpb, Il1rn, and Casp8, showed a significant positive correlation with the degree of NK.Actived, and Icam1 showed a significant negative correlation with B.Cells.Memory. The results of animal experiments significantly demonstrated an upregulation of Irf1, Icam1, Tlr2, Cebpb, and Il1rn. CONCLUSION: Our finding indicated that Irf1, Icam1, Tlr2, Cebpb, and Il1rn are hub genes associated with pyroptosis, and these genes are all associated with different immune cells, so as to provide new targets for the prevention and treatment of IS from the perspective of pyroptosis.

Pyroptosis

Transcriptome analysis under pecan scab infection reveals the molecular mechanisms of the defense response in pecans.

Pecan scab, caused by the fungal pathogen Venturia effusa, is the most devastating disease of pecan (Carya illinoinensis) in the southeastern United States. Resistance to this pathogen is determined by a complex interaction between host genetics and disease pathotype with even field-susceptible cultivars being resistant to most scab isolates. To understand the underlying molecular mechanisms of scab resistance in pecan, we performed a transcriptome analysis of the pecan cultivar, 'Desirable', in response to inoculation with a pathogenic and a non-pathogenic scab isolate at three different time points (24, 48, and 96 hrs. post-inoculation). Differential gene expression and gene ontology enrichment analyses showed contrasting gene expression patterns and pathway enrichment in response to the contrasting isolates with varying pathogenicity. The weighted gene co-expression network analysis of differentially expressed genes detected 11 gene modules. Among them, two modules had significant enrichment of genes involved with defense responses. These genes were particularly upregulated in the resistant reaction at the early stage of fungal infection (24 h) compared to the susceptible reaction. Hub genes in these modules were predominantly related to receptor-like protein kinase activity, signal reception, signal transduction, biosynthesis and transport of plant secondary metabolites, and oxidoreductase activity. Results of this study suggest that the early response of pathogen-related signal transduction and development of cellular barriers against the invading fungus are likely defense mechanisms employed by pecan cultivars against non-virulent scab isolates. The transcriptomic data generated here provide the foundation for identifying candidate resistance genes in pecan against V. effusa and for exploring the molecular mechanisms of disease resistance.

Carya

Proteomic analysis illustrates the potential involvement of dysregulated ribosome-related pathways and disrupted metabolism during retinoic acid-induced cleft palate development.

Recent studies have unveiled disrupted metabolism in the progression of cleft palate (CP), a congenital anomaly characterized by defective fusion of facial structures. Nonetheless, the precise composition of this disrupted metabolism remains elusive, prompting us to identify these components and elucidate primary metabolic irregularities contributing to CP pathogenesis. We established a murine CP model by retinoic acid (RA) treatment and analyzed control and RA-treated embryonic palatal tissues by LC-MS-based proteomic approach. We identified 220 significantly upregulated and 224 significantly downregulated proteins. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed that these differentially expressed proteins (DEPs) were involved in translation, ribosome assembly, mitochondrial function, mRNA binding, as well as key metabolic pathways like oxidative phosphorylation (OXPHOS), glycolysis/gluconeogenesis, and amino acid biosynthesis. These findings suggest that dysregulated ribosome-related pathways and disrupted metabolism play a critical role in CP development. Protein-protein interaction analysis using the STRING database revealed a tightly connected network of DEPs. Furthermore, we identified the top 10 hub proteins in CP using the Cytohubba plugin in Cytoscape. These hub proteins, including RPL8, RPS11, ALB, PA2G4, RPL23, RPS6, CCT7, EGFR, HSPD1, and RPS28, are potentially key regulators of CP pathogenesis. In conclusion, our comprehensive proteomic analysis provides insights into the molecular alterations associated with RA-induced CP in Kun Ming mice. These findings suggest potential therapeutic targets and pathways to understand and prevent congenital craniofacial anomalies.

Cleft Palate

Comparison of the antibiotic resistance mechanisms in a gram-positive and a gram-negative bacterium by gene networks analysis.

Nowadays, the emergence of some microbial species resistant to antibiotics, both gram-positive and gram-negative bacteria, is due to changes in molecular activities, biological processes and their cellular structure in order to survive. The aim of the gene network analysis for the drug-resistant Enterococcus faecium as gram-positive and Salmonella Typhimurium as gram-negative bacteria was to gain insights into the important interactions between hub genes involved in key molecular pathways associated with cellular adaptations and the comparison of survival mechanisms of these two bacteria exposed to ciprofloxacin. To identify the gene clusters and hub genes, the gene networks in drug-resistant E. faecium and S. Typhimurium were analyzed using Cytoscape. Subsequently, the putative regulatory elements were found by examining the promoter regions of the hub genes and their gene ontology (GO) was determined. In addition, the interaction between milRNAs and up-regulated genes was predicted. RcsC and D920_01853 have been identified as the most important of the hub genes in S. Typhimurium and E. faecium, respectively. The enrichment analysis of hub genes revealed the importance of efflux pumps, and different enzymatic and binding activities in both bacteria. However, E. faecium specifically increases phospholipid biosynthesis and isopentenyl diphosphate biosynthesis, whereas S. Typhimurium focuses on phosphorelay signal transduction, transcriptional regulation, and protein autophosphorylation. The similarities in the GO findings of the promoters suggest common pathways for survival and basic physiological functions of both bacteria, including peptidoglycan production, glucose transport and cellular homeostasis. The genes with the most interactions with milRNAs include dpiB, rcsC and kdpD in S. Typhimurium and EFAU004_01228, EFAU004_02016 and EFAU004_00870 in E. faecium, respectively. The results showed that gram-positive and gram-negative bacteria have different mechanisms to survive under antibiotic stress. By deciphering their intricate adaptations, we can develop more effective therapeutic approaches and combat the challenges posed by multidrug-resistant bacteria.

Anti-Bacterial Agents