{"title":"Genetic Variations in the Human Angiotensin-ConvertingEnzyme 2 and Susceptibility to Coronavirus Disease-19.","authors":"Taravat Talebi, Tannaz Masoumi, Katayoun Heshmatzad, Mahshid Hesami, Majid Maleki, Samira Kalayinia","doi":"10.1155/2023/2593199","DOIUrl":"10.1155/2023/2593199","url":null,"abstract":"<p><strong>Background: </strong>Health and economies are both affected by the coronavirus disease-19 (COVID-19) global pandemic. Angiotensin-converting enzyme 2 (<i>ACE2</i>) is a polymorphic enzyme that is a part of the renin-angiotensin system, and it plays a crucial role in viral entry. Previous investigations and studies revealed that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and <i>ACE2</i> have a considerable association. Recently, <i>ACE2</i> variants have been described in human populations in association with cardiovascular and pulmonary conditions. In this study, genetic susceptibility to COVID-19 in different populations was investigated.</p><p><strong>Methods and results: </strong>We evaluated the identified variants based on the predictive performance of 5 deleteriousness-scoring methods and the 2015 American College of Medical Genetics and Genomics (ACMG) guidelines. The results indicated 299 variants within the <i>ACE2</i> gene. The variants were analyzed by different <i>in-silico</i> analysis tools to assess their functional effects. Ultimately, 5 more deleterious variants were found in the <i>ACE2</i> gene.</p><p><strong>Conclusions: </strong>Collecting more information about the variations in binding affinity between SARS-CoV-2 and host-cell receptors due to <i>ACE2</i> variants leads to progress in treatment strategies for COVID-19. The evidence accumulated in this study showed that <i>ACE2</i> variants in different populations may be associated with the genetic susceptibility, symptoms, and outcome of SARS-CoV-2 infection.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2023 ","pages":"2593199"},"PeriodicalIF":1.4,"publicationDate":"2023-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10699955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138802803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Genetics researchPub Date : 2023-11-28eCollection Date: 2023-01-01DOI: 10.1155/2023/5512781
Zhixiang Gao, Shouren Fan
{"title":"The Clinical and Cellular Impact of RBMS2 on the Progression and Prognosis of Kidney Renal Clear Cell Carcinoma.","authors":"Zhixiang Gao, Shouren Fan","doi":"10.1155/2023/5512781","DOIUrl":"10.1155/2023/5512781","url":null,"abstract":"<p><p>This research delves into the implications of the RNA binding motif, single stranded interacting protein 2 (RBMS2)-a gene associated with tumor-suppressing functions-in the context of kidney renal clear cell carcinoma (ccRCC). Through meticulous exploration of online databases, we have identified a negative association between RBMS2 expression and adverse clinico-pathological features, such as advanced TNM stage. Furthermore, our findings indicate that RBMS2 acts as a prognostic predictor for clinical outcomes in ccRCC, evidenced by both univariate and multivariate analyses. Cellular assays have corroborated these findings, revealing that an overexpression of RBMS2 curtails ccRCC cell proliferation and migration. Additionally, our research has unearthed links between RBMS2 and immune infiltration within the ccRCC tumor microenvironment. Collectively, our results underscore the tumor-inhibiting role of RBMS2 in ccRCC and spotlight its potential as a prognostic marker and therapeutic intervention target.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2023 ","pages":"5512781"},"PeriodicalIF":1.4,"publicationDate":"2023-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10697775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138498215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Weimin Li, Jinliang Chen, Chengwei Xiang, Yong Long, Ke Wu, Juan Li
{"title":"The Clinical Relevance and Functional Implications of Thymosin Beta-10 in Glioma","authors":"Weimin Li, Jinliang Chen, Chengwei Xiang, Yong Long, Ke Wu, Juan Li","doi":"10.1155/2023/5517445","DOIUrl":"https://doi.org/10.1155/2023/5517445","url":null,"abstract":"Glioma is a highly aggressive form of brain cancer characterized by limited treatment options and poor patient prognosis. In this study, we aimed to elucidate the oncogenic role of thymosin beta-10 (TMSB10) in glioma through comprehensive analyses of patient data from the TCGA and GTEx databases. Our investigation encompassed several key aspects, including the analysis of patients’ clinical characteristics, survival analysis, in vitro and in vivo functional experiments, and the exploration of correlations between TMSB10 expression and immune cell infiltration. Our findings revealed a significant upregulation of TMSB10 expression in glioma tissues compared to normal brain tissues, with higher expression levels observed in tumors of advanced histological grades. Moreover, we observed positive correlations between TMSB10 expression and patient age, while no significant association with gender was detected. Additionally, TMSB10 exhibited marked elevation in gliomas with wild-type IDH and noncodeletion of 1p/19q. Survival analysis indicated that high TMSB10 expression was significantly associated with worse overall survival, disease-specific survival, and progression-free survival in glioma patients. Functionally, knockdown of TMSB10 in glioma cells resulted in reduced cellular growth rates and impaired tumor growth in xenograft models. Furthermore, our study revealed intriguing correlations between TMSB10 expression and immune cell infiltration within the tumor microenvironment. Specifically, TMSB10 showed negative associations with plasmacytoid dendritic cells (pDC) and γδ T cells (Tgd), while displaying positive correlations with neutrophils and macrophages. These findings collectively provide valuable insights into the oncogenic properties of TMSB10 in glioma, suggesting its potential as a therapeutic target and a biomarker for patient stratification.","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":" 2","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135290928","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pharmacogenetic Approach for the Prevention of Rivaroxaban's ADRs: A Systematic Review and Meta-Analysis.","authors":"Parham Mardi, Bahareh Abbasi, Arman Shafiee, Tara Afsharmoghaddam","doi":"10.1155/2023/6105320","DOIUrl":"10.1155/2023/6105320","url":null,"abstract":"<p><strong>Introduction: </strong>Pharmacogenetics is a potential approach that can be applied to decline the burden of rivaroxaban's ADRs. The current systematic review and meta-analysis aim to identify genetic variants correlated with rivaroxaban exposure and evaluate their importance.</p><p><strong>Methods: </strong>We systematically searched PubMed, Web of Science, and Scopus databases for all observational and interventional studies. The fixed effect method was used to pool the data when the Q-test's <i>p</i> value was higher than 0.1. We used random models when the <i>p</i> value was less than 0.1.</p><p><strong>Results: </strong>Data from ten studies (4721 participants) were analyzed in the current review. Qualitative synthesis from included studies found that two variants of ABCB1 (rs1045642 and rs2032582) and one variant of APOB (rs13306198) are potential contributors to rivaroxaban concentrations. Both wild homozygotes (AA) and heterozygotes (AC) of rs1045642 have significantly lower rivaroxaban concentrations compared to mutated homozygotes (CC) (SMD = 0.516, 95% CI: 0.115 to 0.917; SMD = 0.772, 95% CI: 0.088 to 1.455, respectively). Nevertheless, pooling unadjusted odds ratios did not yield a statistically significant correlation between rivaroxaban ADRs and genetic mutations.</p><p><strong>Conclusion: </strong>This study revealed that being an AC or CC for rs1045642 is attributed to a considerably higher rivaroxaban level in participants using rivaroxaban. That is to say, rs1045642 is a remarkable predictor of rivaroxaban metabolism. We concluded that identifying rs1045642 before drug administration might decrease ADRs although further studies adjusted for potential confounders are strongly suggested.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2023 ","pages":"6105320"},"PeriodicalIF":1.4,"publicationDate":"2023-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10630013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71521183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Genetics researchPub Date : 2023-10-04eCollection Date: 2023-01-01DOI: 10.1155/2023/5565646
Juan Pablo Meza-Espinoza, Valeria Peralta-Leal, Jorge Durán-González, Nelly Macías-Gómez, Anabel Bocanegra-Alonso, Evelia Leal-Ugarte
{"title":"<i>XRCC1</i> R194W and R399Q Polymorphisms and Colorectal Cancer Risk in a Northeastern Mexican Population.","authors":"Juan Pablo Meza-Espinoza, Valeria Peralta-Leal, Jorge Durán-González, Nelly Macías-Gómez, Anabel Bocanegra-Alonso, Evelia Leal-Ugarte","doi":"10.1155/2023/5565646","DOIUrl":"10.1155/2023/5565646","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most common cancers worldwide. Its etiopathogenesis is complex, mainly influenced by genetic instability caused by the accumulation of mutations. The <i>XRCC1</i> gene, which is involved in DNA repair, has been associated with CRC through the R194W (C194T) and R399Q (G399A) polymorphisms, but the results are inconsistent. Here, we analyzed the association of these polymorphisms with sporadic CRC in a northeastern Mexican population, including 155 male CRC patients and 155 male controls. Genotyping was performed using the RFLP method. An association with CRC was found for the 399A allele (G vs A; OR = 1.48 (1.03-2.13), <i>P</i>=0.034) and for the 399AA genotype in a codominant model (AA vs GG; OR = 3.11 (1.06-9.10), <i>P</i>=0.031). In contrast, there were no significant differences between CRC patients and controls for the C194T polymorphism (C vs T; OR = 0.82 (0.52-1.31), <i>P</i>=0.41). These results are consistent with many similar studies, but further research is needed to verify whether the <i>XRCC1</i> R194W and R399Q polymorphisms play a role in CRC etiology. The functional significance of these polymorphisms is unclear, but some studies suggest that they influence DNA repair capacity and, thus, cancer risk.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2023 ","pages":"5565646"},"PeriodicalIF":1.4,"publicationDate":"2023-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10567464/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41199045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Genetics researchPub Date : 2023-10-04eCollection Date: 2023-01-01DOI: 10.1155/2023/9999660
Ghazanfar Ali, Sadia Sadia, Syeda Ain-Ul-Batool, Zahid Azeem, Naheed Bashir Awan, Syed Akif Raza Kazmi, Zia- Ur-Rehman, Zeeshan Anjum, Fazal- Ur-Rehman, Abdul Wali, Kafaitullah Khan, Nasib Zaman, Muhammad Ayub, Muhammad Sajid, Noor Hassan
{"title":"A Recurrent Nonsense Mutation in NECTIN4 Underlying Ectodermal Dysplasia-Syndactyly Syndrome with a Novel Phenotype in a Consanguineous Kashmiri Family.","authors":"Ghazanfar Ali, Sadia Sadia, Syeda Ain-Ul-Batool, Zahid Azeem, Naheed Bashir Awan, Syed Akif Raza Kazmi, Zia- Ur-Rehman, Zeeshan Anjum, Fazal- Ur-Rehman, Abdul Wali, Kafaitullah Khan, Nasib Zaman, Muhammad Ayub, Muhammad Sajid, Noor Hassan","doi":"10.1155/2023/9999660","DOIUrl":"10.1155/2023/9999660","url":null,"abstract":"<p><p>EDSS1, a syndrome characterized by ectodermal dysplasia-syndactyly, is inherited in an autosomal recessive manner due to mutations in the NECTIN4/PVRL4 gene. Clinical manifestations of the syndrome include defective nail plate, sparse to absent scalp and body hair, spaced teeth with enamel hypoplasia, and bilateral cutaneous syndactyly in the fingers and toes. Here, we report a consanguineous family of Kashmiri origin presenting features of EDSS1. Using whole exome sequencing, we found a recurrent nonsense mutation (NM_030916: c.181C > T, p.(Gln61 <i>∗</i>)) in the NECTIN4 gene. The variant segregated perfectly with the disorder within the family. The candidate variant was absent in 50 in-house exomes pertaining to other disorders from the same population. In addition to the previously reported clinical phenotype, an upper lip cleft was found in one of the affected members as a novel phenotype that is not reported by previous studies in EDSS1 patients. Therefore, the study presented here, which was conducted on the Kashmiri population, is the first to document a NECTIN4 mutation associated with the upper lip cleft as a novel phenotype. This finding broadens the molecular and phenotypic spectrum of EDSS1.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2023 ","pages":"9999660"},"PeriodicalIF":1.4,"publicationDate":"2023-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10567209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41199046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Genetics researchPub Date : 2023-09-21eCollection Date: 2023-01-01DOI: 10.1155/2023/5513812
Jing Wei, Xin Wang, Kai Jiao
{"title":"Orthodenticle Homeobox OTX1 Promotes Papillary Thyroid Carcinoma Progression and Is a Potential Prognostic Biomarker.","authors":"Jing Wei, Xin Wang, Kai Jiao","doi":"10.1155/2023/5513812","DOIUrl":"10.1155/2023/5513812","url":null,"abstract":"<p><p>Papillary thyroid carcinoma (PTC) is the most common type of thyroid neoplasms, characterized by evidence of follicular cell differentiation. Orthodenticle homeobox 1 (OTX1) is a transcription factor which has been implicated in numerous diseases, including malignancies. The objective of this research was to explore the function of OTX1 in PTC. Immunohistochemistry (IHC) was employed to determine the protein level of OTX1 in PTC specimens. Cell viability was assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Furthermore, a xenograft model on nude mice was established to investigate in vivo effects of OTX1. Our results revealed that OTX1 was significantly upregulated within specific PTC tissues and was remarkably correlated with unfavorable clinical outcomes in PTC. Silencing OTX1 resulted in a significant inhibition in cell viability and suppressed cell proliferation. In addition, in vivo experiments demonstrated that OTX1 silencing resulted in a significant suppression of tumor growth in nude mice. Collectively, these results suggest that OTX1 may play crucial roles in promoting PTC progression.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2023 ","pages":"5513812"},"PeriodicalIF":1.4,"publicationDate":"2023-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10539079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41121808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Advanced Glycation End Products' Receptor DNA Methylation Associated with Immune Infiltration and Prognosis of Lung Adenocarcinoma and Lung Squamous Cell Carcinoma.","authors":"Jun Yang, Mingqiang Lin, Mengyan Zhang, Zhiping Wang, Hancui Lin, Yilin Yu, Qunhao Zheng, Xiaohui Chen, Yahua Wu, Qiwei Yao, Jiancheng Li","doi":"10.1155/2023/7129325","DOIUrl":"10.1155/2023/7129325","url":null,"abstract":"<p><strong>Background: </strong>Advanced glycation end products' receptor (AGER) is a multiligand receptor that interacts with a wide range of ligands. Previous studies have shown that abnormal AGER expression is closely related to immune infiltration and tumorigenesis. However, the AGER DNA methylation relationship between prognosis and infiltrating immune cells in LUAD and LUSC is still unclear.</p><p><strong>Methods: </strong>AGER expression in pan-cancer was obtained by using the UALCAN databases. Kaplan-Meier plotter showed the correlation of <i>AGER</i> mRNA expression levels and clinicopathological parameters. The protein expression levels for AGER were derived from Human Protein Atlas Database Analysis. The copy number, somatic mutation, and DNA methylation of AGER were presented with UCSC Xena database. TIMER platform and TISIDB website were used to show the correlation between <i>AGER</i> expression and tumor immune cell infiltration level.</p><p><strong>Results: </strong>The expression level of <i>AGER</i> was significantly reduced in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Low expression of <i>AGER</i> was significantly correlated with histology, stage, lymph node metastasis, and tumor protein 53 (TP53) mutation and could be used as a potential indicator of poor prognosis of LUAD and LUSC. Moreover, <i>AGER</i> expression was positively correlated with the infiltrating immune cells. Further analysis showed that copy number variation (CNV), mutation, and DNA methylation were involved in AGER downregulation. In addition, we also found that hypermethylated AGER was significantly correlated with tumor-infiltrating lymphocytes.</p><p><strong>Conclusion: </strong>AGER may be a candidate for the prognostic biomarker of LUAD and LUSC related to tumor immune microenvironment.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2023 ","pages":"7129325"},"PeriodicalIF":1.4,"publicationDate":"2023-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10368508/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9925124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Genetics researchPub Date : 2023-03-31eCollection Date: 2023-01-01DOI: 10.1155/2023/1230182
Ning Li, Haifei Song, Zhiqin Chen, Chen Chen, Ming Quan
{"title":"Novel KDM2B/SAV1 Signaling Pathway Promotes the Progression of Gastric Cancer.","authors":"Ning Li, Haifei Song, Zhiqin Chen, Chen Chen, Ming Quan","doi":"10.1155/2023/1230182","DOIUrl":"10.1155/2023/1230182","url":null,"abstract":"<p><p>Salvador homologue 1 (SAV1), which is reported to act as a tumor suppressor in different types of cancer, is one of the key components of the Hippo pathway. However, the expression and mechanisms of SAV1 in the development and progression of gastric cancer (GC) remain to be elucidated. Immunohistochemistry (IHC) was performed in the present study to assess the expression levels of SAV1 and lysine-specific demethylase 2B (KDM2B) in GC tissues. The biological effects of SAV1 on GC cell proliferation, migration, and invasion were studied <i>in vitro</i>. KDM2B transcriptionally regulates SAV1 expression in several GC cell lines, and molecular experiments were performed to investigate underlying mechanisms. The expression level of SAV1 was significantly decreased in GC tissues and cell lines, negatively associated with tumor invasion depth, lymph node metastasis, and TNM stage, and positively associated with the overall survival of patients with GC. SAV1 overexpression inhibited the proliferation, migration, and invasion of GC cells. Further mechanistic studies revealed that KDM2B transcriptionally regulated SAV1 expression and further regulated the Hippo signaling pathway. To conclude, the present study demonstrated that KDM2B transcriptionally regulated SAV1 expression and promoted GC progression.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2023 ","pages":"1230182"},"PeriodicalIF":1.4,"publicationDate":"2023-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10081913/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9637398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Genetics researchPub Date : 2023-03-23eCollection Date: 2023-01-01DOI: 10.1155/2023/8511036
Eun Jung Sohn
{"title":"Functional Analysis of Monkeypox and Interrelationship between Monkeypox and COVID-19 by Bioinformatic Analysis.","authors":"Eun Jung Sohn","doi":"10.1155/2023/8511036","DOIUrl":"10.1155/2023/8511036","url":null,"abstract":"<p><p>The outbreak of monkeypox may be considered a novel and urgent threat after the coronavirus disease (COVID-19). No wide-ranging studies have been conducted on this disease since it was first reported. We systematically assessed the functional role of gene expression in cells infected with the monkeypox virus using transcriptome profiling and compared the functional relation with that of COVID-19. Based on the Gene Expression Omnibus database, we obtained 212 differentially expressed genes (DEGs) of GSE36854 and GSE21001 of monkeypox datasets. Enrichment analyses, including KEGG and gene ontology (GO) analyses, were performed to identify the common function of 212 DEGs of GSE36854 and GSE21001. CytoHubba and Molecular Complex Detection were performed to determine the core genes after a protein-protein interaction (PPI). Metascape/COVID-19 was used to compare DEGs of monkeypox and COVID-19. GO analysis of 212 DEGs of GSE36854 and GSE21001 for monkeypox infection showed cellular response to cytokine stimulus, cell activation, and cell differentiation regulation. KEGG analysis of 212 DEGs of GSE36854 and GSE21001 for monkeypox infection showed involvement of monkeypox in COVID-19, cytokine-cytokine receptor interaction, inflammatory bowel disease, atherosclerosis, TNF signaling, and T cell receptor signaling. By comparing our data with published transcriptome of severe acute respiratory syndrome coronavirus 2 infections in other cell lines, the common function of monkeypox and COVID-19 includes cytokine signaling in the immune system, TNF signaling, and MAPK cascade regulation. Thus, our data suggest that the molecular connections identified between COVID-19 and monkeypox elucidate the causes of monkeypox.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2023 ","pages":"8511036"},"PeriodicalIF":1.5,"publicationDate":"2023-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10063359/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9264179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}