Pub Date : 2025-08-01DOI: 10.1016/j.meomic.2025.100047
Ali Khan, Sara Khan, Muhammad Rahiyab, Salman Khan, Zabih Ullah, Syed Shujait Ali
Bovine alphaherpesvirus 2 (BoHV-2), a major pathogen in cattle, belongs to the Herpesviridae family. In this work, we designed a vaccine against BoHV-2 using its envelope glycoprotein B (gB) and glycoprotein H. In this work, computational methods were utilized for predicting the B and T lymphocyte epitopes with striking results in their antigenicity and low allergenicity. Thereafter, the vaccine design stability tests showed that it was physicochemically stable. Molecular docking and molecular dynamics simulation analyses validated its further efficacy. The docking results demonstrated 11 hydrogen bonds coupled with one salt bridge between the vaccine and TLR3 while PRODIGY analysis suggested a binding free energy (ΔG) of −10.7 kcal/mol alongside a dissociation constant (kDa) of 1.5e-08. In silico cloning demonstrations showed effective expression levels together with immune simulation predictions, suggesting robust immunological responses. However, this study has certain limitations, such as the experimental validation. Future in vivo and in vitro studies are required to confirm the immunogenicity and safety of the in-silico designed vaccine construct.
{"title":"Designing a highly antigenic multi epitope subunit vaccine against Bovine alpha herpes virus 2 targeting glycoprotein B and H: A reverse vaccinology approach","authors":"Ali Khan, Sara Khan, Muhammad Rahiyab, Salman Khan, Zabih Ullah, Syed Shujait Ali","doi":"10.1016/j.meomic.2025.100047","DOIUrl":"10.1016/j.meomic.2025.100047","url":null,"abstract":"<div><div>Bovine alphaherpesvirus 2 (BoHV-2), a major pathogen in cattle, belongs to the <em>Herpesviridae</em> family. In this work, we designed a vaccine against BoHV-2 using its envelope glycoprotein B (gB) and glycoprotein H. In this work, computational methods were utilized for predicting the B and T lymphocyte epitopes with striking results in their antigenicity and low allergenicity. Thereafter, the vaccine design stability tests showed that it was physicochemically stable. Molecular docking and molecular dynamics simulation analyses validated its further efficacy. The docking results demonstrated 11 hydrogen bonds coupled with one salt bridge between the vaccine and TLR3 while PRODIGY analysis suggested a binding free energy (ΔG) of −10.7 kcal/mol alongside a dissociation constant (kDa) of 1.5e-08. In silico cloning demonstrations showed effective expression levels together with immune simulation predictions, suggesting robust immunological responses. However, this study has certain limitations, such as the experimental validation. Future <em>in vivo</em> and <em>in vitro</em> studies are required to confirm the immunogenicity and safety of the in-silico designed vaccine construct.</div></div>","PeriodicalId":100914,"journal":{"name":"Medicine in Omics","volume":"14 ","pages":"Article 100047"},"PeriodicalIF":0.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144925352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-07-08DOI: 10.1016/j.meomic.2025.100046
Yanjun Liang , Xiao Zhu
Alternative splicing (AS) is pivotal in gene expression regulation and protein diversity generation. Suppression of aberrant AS holds promise in cancer management. Utilizing zebrafish-human homologous genes, we investigated AS events across 33 tumor types from TCGA, employing Cox regression analyses to identify prognostic AS events. A risk-scoring model distinguished high and low-risk groups, revealing differences in survival, tumor microenvironment, and immune cell infiltration. Notably, Complement C1q C Chain (C1QC), DENND5A, HP, IRF5, and LRP1 were associated with poor prognosis and immune infiltration. Mendelian randomization confirmed the protective role of C1QC across cancers, further supported by Bayesian Weighted Mendelian Randomization. Leveraging zebrafish homologs enhances our understanding of AS mechanisms and potential therapeutic targets in cancer biology.
{"title":"Analysis of zebrafish homologs within the human genome provides valuable insights into exploring pan-cancer alternative splicing events as prognostic markers and therapeutic targets","authors":"Yanjun Liang , Xiao Zhu","doi":"10.1016/j.meomic.2025.100046","DOIUrl":"10.1016/j.meomic.2025.100046","url":null,"abstract":"<div><div>Alternative splicing (AS) is pivotal in gene expression regulation and protein diversity generation. Suppression of aberrant AS holds promise in cancer management. Utilizing zebrafish-human homologous genes, we investigated AS events across 33 tumor types from TCGA, employing Cox regression analyses to identify prognostic AS events. A risk-scoring model distinguished high and low-risk groups, revealing differences in survival, tumor microenvironment, and immune cell infiltration. Notably, Complement C1q C Chain (C1QC), DENND5A, HP, IRF5, and LRP1 were associated with poor prognosis and immune infiltration. Mendelian randomization confirmed the protective role of C1QC across cancers, further supported by Bayesian Weighted Mendelian Randomization. Leveraging zebrafish homologs enhances our understanding of AS mechanisms and potential therapeutic targets in cancer biology.</div></div>","PeriodicalId":100914,"journal":{"name":"Medicine in Omics","volume":"14 ","pages":"Article 100046"},"PeriodicalIF":0.0,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144680574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-26DOI: 10.1016/j.meomic.2025.100045
Xiao Zhu , Zhuolong Xiong
Background
Lung adenocarcinoma (LUAD) is characterized by low overall survival rates. This research aims to explore the association between long non-coding RNAs (lncRNAs) and chromatin histone methylation/demethylation modifiers in LUAD.
Methods
Datasets from The Cancer Genome Atlas (TCGA), Molecular Signatures Database (MSigDB), and IEU Open genome-wide association studies (GWAS) database were analyzed. A prognostic risk model for LUAD was developed based on 32 lncRNAs linked to histone modification. The relationship between lncRNAs and the high-risk group of lung cancer was evaluated, and GO/KEGG analysis was conducted to investigate the connection between chromatin histone modification-related lncRNAs and biological processes/pathways. Mendelian Randomization methods, including Inverse Variance Weighted (IVW) and Bayesian Weighted Mendelian Randomization (BWMR), were employed to validate the GO/KEGG results. MR-Egger intercept test, Cochran’s Q test, and leave-one-out Analysis were utilized to assess the sensitivity of Mendelian Randomization analysis. Tumor mutation burden (TMB) analysis was performed to evaluate the prognostic impact of high-risk patients with high TMB.
Results
Identified lncRNAs, including AC025741.1 and NHS-AS1, demonstrated strong associations with the high-risk group. GO/KEGG analysis revealed significant correlations between chromatin histone modification-related lncRNAs and microtubule-based movement and cytochrome enzyme P450. Response to the renin-angiotensin agents is a protective factor for lung cancer, while response to glucocorticoids is a risk factor for lung cancer. Immunomarkers MDSC, CAF, and Exclusion showed positive correlations with the risk score, and the combined effects of CAF and MDSC were found to play a pivotal role in LUAD development and progression.
Conclusion
Our study not only establishes a promising LUAD prognostic risk model with potential implications for immunotherapy but also identifies lncRNAs as immune markers for LUAD immunotherapy. Additionally, we validate the causal relationship between chromatin histone methylation-related pathways and lung cancer, bolstering our understanding from a genetic perspective and opening avenues for targeted interventions in LUAD treatment.
{"title":"Multi-omics integration reveals chromatin-associated lncRNA prognostic model in lung adenocarcinoma: Bridging GWAS, transcriptome and clinical outcomes","authors":"Xiao Zhu , Zhuolong Xiong","doi":"10.1016/j.meomic.2025.100045","DOIUrl":"10.1016/j.meomic.2025.100045","url":null,"abstract":"<div><h3>Background</h3><div>Lung adenocarcinoma (LUAD) is characterized by low overall survival rates. This research aims to explore the association between long non-coding RNAs (lncRNAs) and chromatin histone methylation/demethylation modifiers in LUAD.</div></div><div><h3>Methods</h3><div>Datasets from The Cancer Genome Atlas (TCGA), Molecular Signatures Database (MSigDB), and IEU Open genome-wide association studies (GWAS) database were analyzed. A prognostic risk model for LUAD was developed based on 32 lncRNAs linked to histone modification. The relationship between lncRNAs and the high-risk group of lung cancer was evaluated, and GO/KEGG analysis was conducted to investigate the connection between chromatin histone modification-related lncRNAs and biological processes/pathways. Mendelian Randomization methods, including Inverse Variance Weighted (IVW) and Bayesian Weighted Mendelian Randomization (BWMR), were employed to validate the GO/KEGG results. MR-Egger intercept test, Cochran’s Q test, and leave-one-out Analysis were utilized to assess the sensitivity of Mendelian Randomization analysis. Tumor mutation burden (TMB) analysis was performed to evaluate the prognostic impact of high-risk patients with high TMB.</div></div><div><h3>Results</h3><div>Identified lncRNAs, including AC025741.1 and NHS-AS1, demonstrated strong associations with the high-risk group. GO/KEGG analysis revealed significant correlations between chromatin histone modification-related lncRNAs and microtubule-based movement and cytochrome enzyme P450. Response to the renin-angiotensin agents is a protective factor for lung cancer, while response to glucocorticoids is a risk factor for lung cancer. Immunomarkers MDSC, CAF, and Exclusion showed positive correlations with the risk score, and the combined effects of CAF and MDSC were found to play a pivotal role in LUAD development and progression.</div></div><div><h3>Conclusion</h3><div>Our study not only establishes a promising LUAD prognostic risk model with potential implications for immunotherapy but also identifies lncRNAs as immune markers for LUAD immunotherapy. Additionally, we validate the causal relationship between chromatin histone methylation-related pathways and lung cancer, bolstering our understanding from a genetic perspective and opening avenues for targeted interventions in LUAD treatment.</div></div>","PeriodicalId":100914,"journal":{"name":"Medicine in Omics","volume":"14 ","pages":"Article 100045"},"PeriodicalIF":0.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144604159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Alzheimer’s disease (AD) is a neurodegenerative disorder responsible for 70–80 % of dementia cases. Aluminum, a neurotoxicant, accelerates AD progression through oxidative stress and neuroinflammation. Many phytochemicals have shown promise as alternative AD therapies. This study investigated the therapeutic effects of Persea americana (PA) and Tabebuia rosea (TR) ethanolic leaf extracts in aluminum chloride (AlCl3)-induced AD in male rats. GC–MS analysis identified phytocompounds in the extracts. Forty-two male rats (70–100 g) were divided into six groups: control, AlCl3-only, TR-treated, PA-treated, combined extracts, and donepezil-treated (standard AD drug) groups. Biochemical and histopathological analyses were conducted on brain tissues. In silico analysis docked Beta-secretase (BACE1) against Elenbecestat and extracted phytochemicals. AlCl3 exposure significantly increased acetylcholinesterase (AChE) activity and malondialdehyde (MDA) levels while reducing glutathione (GSH) levels, with notable brain histopathology. PA and TR treatment reversed these effects, lowering AChE and MDA levels while increasing GSH. In silico analysis revealed that ethyl (9E,12E)-octadeca-9,12-dienoate and 9-octadecenoic acid, ethyl ester, exhibited superior docking scores and binding energies compared to Elenbecestat. These findings suggest PA and TR extracts as potential alternative treatments for AD.
{"title":"Neuroprotective effects of Persea americana and Tabebuia rosea ethanolic extracts against aluminum chloride-induced Alzheimer’s disease in rat model","authors":"Olayinka Fisayo Onifade , Oluwasayo Peter Abodunrin , Esther Omolara Oyeneye , Ebubechukwu Goodness Chigozie , Abdusalam Gbemisola Arafa , Benjamen Olujide Okunlola","doi":"10.1016/j.meomic.2025.100044","DOIUrl":"10.1016/j.meomic.2025.100044","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is a neurodegenerative disorder responsible for 70–80 % of dementia cases. Aluminum, a neurotoxicant, accelerates AD progression through oxidative stress and neuroinflammation. Many phytochemicals have shown promise as alternative AD therapies. This study investigated the therapeutic effects of <em>Persea americana</em> (PA) and <em>Tabebuia rosea</em> (TR) ethanolic leaf extracts in aluminum chloride (AlCl<sub>3</sub>)-induced AD in male rats. GC–MS analysis identified phytocompounds in the extracts. Forty-two male rats (70–100 g) were divided into six groups: control, AlCl<sub>3</sub>-only, TR-treated, PA-treated, combined extracts, and donepezil-treated (standard AD drug) groups. Biochemical and histopathological analyses were conducted on brain tissues. <em>In silico</em> analysis docked Beta-secretase (BACE1) against Elenbecestat and extracted phytochemicals. AlCl<sub>3</sub> exposure significantly increased acetylcholinesterase (AChE) activity and malondialdehyde (MDA) levels while reducing glutathione (GSH) levels, with notable brain histopathology. PA and TR treatment reversed these effects, lowering AChE and MDA levels while increasing GSH. <em>In silico</em> analysis revealed that ethyl (9E,12E)-octadeca-9,12-dienoate and 9-octadecenoic acid, ethyl ester, exhibited superior docking scores and binding energies compared to Elenbecestat. These findings suggest PA and TR extracts as potential alternative treatments for AD.</div></div>","PeriodicalId":100914,"journal":{"name":"Medicine in Omics","volume":"14 ","pages":"Article 100044"},"PeriodicalIF":0.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144535115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01DOI: 10.1016/j.meomic.2025.100041
Xiaohui Shi , Xiao Zhu , Dongpei Li
Background
Epigenetic reprogramming plays a crucial role in the progression of uveal melanoma (UM). RNA methylation constitutes more than 60% of all RNA modifications, with N6-methyladenosine (m6A) being the most prevalent RNA modification in higher organisms. This study aimed to investigate the construction of the m6A regulatory factor modification model and its assessment of UM clinical prognosis.
Methods
The expression levels of 23 m6A regulators in The Cancer Genome Atlas (TCGA) were analyzed, and the survival rate was assessed based on TCGA clinicopathological data. Consistent cluster analysis was performed to evaluate different m6A scores in tumor mutation burden (TMB) and to predict the correlation between m6A scores and UM prognosis.
Results
Various expression patterns of m6A regulators were observed in UM tumors, and multiple m6A genes were found to be correlated with prognosis. Through consistent cluster analysis, three distinct m6A modification patterns were identified. The overlapping differentially expressed genes (DEGs) among the three m6A clusters were screened, leading to the establishment of three different subgroups. Among these subgroups, cluster B exhibited the most favorable prognosis. Based on the m6A score derived from DEGs, UM patients could be categorized into high-scoring subgroup and low-scoring subgroup subgroups. Importantly, patients with higher m6A scores demonstrated prolonged survival and improved clinical characteristics. Furthermore, the study established an association between the m6A score and TMB, suggesting that the m6A score may serve as a potential prognostic predictor for UM patients.
Conclusion
We conducted a screening of DEGs from the m6A cluster and categorized them into three distinct clusters for analysis of m6A scores. Subsequently, we developed a highly predictive model with prognostic value. This study will contribute to our understanding of the overall impact of m6A modification patterns on the progression of UM.
{"title":"Omics-based evaluation of m6A modification patterns in uveal melanoma and their prognostic implications","authors":"Xiaohui Shi , Xiao Zhu , Dongpei Li","doi":"10.1016/j.meomic.2025.100041","DOIUrl":"10.1016/j.meomic.2025.100041","url":null,"abstract":"<div><h3>Background</h3><div>Epigenetic reprogramming plays a crucial role in the progression of uveal melanoma (UM). RNA methylation constitutes more than 60% of all RNA modifications, with N6-methyladenosine (m6A) being the most prevalent RNA modification in higher organisms. This study aimed to investigate the construction of the m6A regulatory factor modification model and its assessment of UM clinical prognosis.</div></div><div><h3>Methods</h3><div>The expression levels of 23 m6A regulators in The Cancer Genome Atlas (TCGA) were analyzed, and the survival rate was assessed based on TCGA clinicopathological data. Consistent cluster analysis was performed to evaluate different m6A scores in tumor mutation burden (TMB) and to predict the correlation between m6A scores and UM prognosis.</div></div><div><h3>Results</h3><div>Various expression patterns of m6A regulators were observed in UM tumors, and multiple m6A genes were found to be correlated with prognosis. Through consistent cluster analysis, three distinct m6A modification patterns were identified. The overlapping differentially expressed genes (DEGs) among the three m6A clusters were screened, leading to the establishment of three different subgroups. Among these subgroups, cluster B exhibited the most favorable prognosis. Based on the m6A score derived from DEGs, UM patients could be categorized into high-scoring subgroup and low-scoring subgroup subgroups. Importantly, patients with higher m6A scores demonstrated prolonged survival and improved clinical characteristics. Furthermore, the study established an association between the m6A score and TMB, suggesting that the m6A score may serve as a potential prognostic predictor for UM patients.</div></div><div><h3>Conclusion</h3><div>We conducted a screening of DEGs from the m6A cluster and categorized them into three distinct clusters for analysis of m6A scores. Subsequently, we developed a highly predictive model with prognostic value. This study will contribute to our understanding of the overall impact of m6A modification patterns on the progression of UM.</div></div>","PeriodicalId":100914,"journal":{"name":"Medicine in Omics","volume":"13 ","pages":"Article 100041"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144169424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01DOI: 10.1016/j.meomic.2025.100042
Yaqi Huang , Xiao Zhu , Dongpei Li
The development and prognosis of acute myeloid leukemia (AML) are influenced by multiple factors. This study utilized bioinformatics analysis to explore differentially expressed genes (DEGs) in acute myeloid leukemia (AML) and non-tumor tissues, evaluating their prognostic significance. Target gene data from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases were extracted for analysis. Over 100 DEGs were identified, with MIR9-1 exhibiting downregulated expression in AML. Survival analysis revealed significant differences in overall survival rates between subgroups, with Cluster 2 showing better outcomes. Notable DEGs, including DEFA1B, FLT3LG, CUX1, and ZMYM2, were identified. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis highlighted relevant signaling pathways. Mendelian Randomization (MR) analysis unveiled a negative correlation between the “transcriptional misregulation in cancer pathway” and “hypermethylation of CpG island pathway” with AML. Sensitivity analysis demonstrated no heterogeneity or pleiotropy. Bayesian Weighted Mendelian Randomization (BWMR) validated MR results. Overall, this study identified potential therapeutic targets like FLT3LG, elucidated key genes for AML prognosis, and revealed protective roles of pathways through comprehensive bioinformatics analysis and Mendelian randomization.
{"title":"Uncovering prognostic markers and therapeutic targets in acute myeloid leukemia: Insights from differential gene expression and Mendelian randomization analysis","authors":"Yaqi Huang , Xiao Zhu , Dongpei Li","doi":"10.1016/j.meomic.2025.100042","DOIUrl":"10.1016/j.meomic.2025.100042","url":null,"abstract":"<div><div>The development and prognosis of acute myeloid leukemia (AML) are influenced by multiple factors. This study utilized bioinformatics analysis to explore differentially expressed genes (DEGs) in acute myeloid leukemia (AML) and non-tumor tissues, evaluating their prognostic significance. Target gene data from The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases were extracted for analysis. Over 100 DEGs were identified, with MIR9-1 exhibiting downregulated expression in AML. Survival analysis revealed significant differences in overall survival rates between subgroups, with Cluster 2 showing better outcomes. Notable DEGs, including DEFA1B, FLT3LG, CUX1, and ZMYM2, were identified. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis highlighted relevant signaling pathways. Mendelian Randomization (MR) analysis unveiled a negative correlation between the “transcriptional misregulation in cancer pathway” and “hypermethylation of CpG island pathway” with AML. Sensitivity analysis demonstrated no heterogeneity or pleiotropy. Bayesian Weighted Mendelian Randomization (BWMR) validated MR results. Overall, this study identified potential therapeutic targets like FLT3LG, elucidated key genes for AML prognosis, and revealed protective roles of pathways through comprehensive bioinformatics analysis and Mendelian randomization.</div></div>","PeriodicalId":100914,"journal":{"name":"Medicine in Omics","volume":"13 ","pages":"Article 100042"},"PeriodicalIF":0.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144184894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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