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Lv, J., H. Liu, J. Su, X. Wu, H. Liu, B. Li, X. Xiao, F. Wang, Q. Wu, and Y. Zhang. "DiseaseMeth: a human disease methylation database." Nucleic Acids Research 40, no. D1 (December 1, 2011): D1030—D1035. http://dx.doi.org/10.1093/nar/gkr1169.
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Xing, Jie, Ruiyang Zhai, Cong Wang, Honghao Liu, Jiaqi Zeng, Dianshuang Zhou, Mengyan Zhang, et al. "DiseaseMeth version 3.0: a major expansion and update of the human disease methylation database." Nucleic Acids Research 50, no. D1 (November 18, 2021): D1208—D1215. http://dx.doi.org/10.1093/nar/gkab1088.
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Abstract DNA methylation has a growing potential for use as a biomarker because of its involvement in disease. DNA methylation data have also substantially grown in volume during the past 5 years. To facilitate access to these fragmented data, we proposed DiseaseMeth version 3.0 based on DiseaseMeth version 2.0, in which the number of diseases including increased from 88 to 162 and High-throughput profiles samples increased from 32 701 to 49 949. Experimentally confirmed associations added 448 pairs obtained by manual literature mining from 1472 papers in PubMed. The search, analyze and tools sections were updated to increase performance. In particular, the FunctionSearch now provides for the functional enrichment of genes from localized GO and KEGG annotation. We have also developed a unified analysis pipeline for identifying differentially DNA methylated genes (DMGs) from the original data stored in the database. 22 718 DMGs were found in 99 diseases. These DMGs offer application in disease evaluation using two self-developed online tools, Methylation Disease Correlation and Cancer Prognosis & Co-Methylation. All query results can be downloaded and can also be displayed through a box plot, heatmap or network module according to whichever search section is used. DiseaseMeth version 3.0 is freely available at http://diseasemeth.edbc.org/.
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Xiong, Yichun, Yanjun Wei, Yue Gu, Shumei Zhang, Jie Lyu, Bin Zhang, Chuangeng Chen, et al. "DiseaseMeth version 2.0: a major expansion and update of the human disease methylation database." Nucleic Acids Research 45, no. D1 (November 29, 2016): D888—D895. http://dx.doi.org/10.1093/nar/gkw1123.
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Zhao, Xiaorong, Wenzhuo Wang, Dandan Li, Qingjuan Li, Yuxuan Zhang, and Bo Niu. "SHCBP1: A Novel Potential Molecular Target for Pan- Cancer Therapy." Neurological Disorders and Stroke International 4, no. 1 (May 10, 2022): 1–11. http://dx.doi.org/10.25107/2641-1407-v4-id1026.
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Purpose: Although many experimentally validated evidence and clinical data support the link between SHCBP1 (SHC-Binding and Spindle-Associated 1) and cancer, there is no pan-cancer analysis available. Based on various databases, we analyzed the roles assumed by SHCBP1 in different cancers to provide new targets for cancer therapy. Methods: We used versatile public databases such as TIMER, Interactive Analysis of Gene Expression Profile, 2nd Edition (GEPIA), UALCAN, The Cancer Genome Atlas (TCGA), cBioPortal, Clinical Bioinformatics Assistant, DiseaseMeth, TISIDB, Human Protein Atlas (HPA), STRING and Database for Annotation, Visualization, and Integrated Discovery (DAVID) to analyze SHCBP1 expression, mutation, methylation in tumors, as well as its survival analysis, tumor-immune interactions and functional networks. Results: SHCBP1 was highly expressed in most tumors leading to poor prognosis and the degree of expression was positively correlated with the degree of infiltration by activated memory CD4+ T cells. We observed cancer-associated fibroblast infiltration in Breast Invasive Carcinoma (BRCA), Renal Clear Cell Carcinoma (KIRC) and Thyroid Cancer (THCA). Protein kinase activity and microtubules can influence gene enrichment, while "cell cycle", "oocyte meiosis" and "viral carcinogenesis" are possible pathways of SHCBP1 involvement in tumorigenesis. Conclusion: Altogether, our first pan-cancer analysis of SHCBP1 demonstrated its potential as a biomarker for tumor prognosis diagnosis or as a molecular target for immunotherapy.
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Tang, Lulu, ling Huang, and yingtao Lai. "Network pharmacology and bioinformatics analyses identify the intersection genes and mechanism of Huang Bai for recurrent aphthous stomatitis." International Journal of Immunopathology and Pharmacology 36 (January 2022): 039463202211291. http://dx.doi.org/10.1177/03946320221129134.
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Recurrent aphthous stomatitis (RAS) are complex inflammatory diseases caused by multi-factors, which severely impact patient quality of life. However, there is still no effective treatment method for RAS without side effects. Traditionally, Cortex Phellodendri known as “Huang Bai” was used to treat RAS for antibacterial and anti-inflammatory properties in China. Network pharmacology methods and bioinformatics analysis were utilized to search and fish incorporating target. Network analysis and silico validation were used to discover the pharmacological mechanisms of “Huang Bai” for the treatment of RAS. A total of 25 active ingredients in HB, 200 drug targets, and 578 differentially expressed genes (DEGs) between Recurrent aphthous stomatitis and normal samples were obtained. The Gene Ontology enrichment analysis revealed that the immune response was the most significantly enriched term within the DEGs. The KEGG pathway analysis identified 60 significant pathways, most of which involved in the inhibition of inflammation and regulation of immunological response. The functions are dependent on a multi-pathway, particularly the TNF signaling pathway and the HIF-1 signaling pathway. We identified six hub genes in the PPI network, most of which were validated as highly expressed in oral ulcers by DiseaseMeth databases. In addition, molecular docking displayed that the primary molecule combined well with the key targets. “Huang Bai” contains potential anti-RAS active compounds. This study reflects the multi-component multi-target multi-pathway action characteristics of “Huang Bai.” Our study provides potential biomarkers or treatment targets for further research.
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Qian, Xiang, Zhuo Chen, Sha Sha Chen, Lu Ming Liu, and Ai Qin Zhang. "Integrated Analyses Identify Immune-Related Signature Associated with Qingyihuaji Formula for Treatment of Pancreatic Ductal Adenocarcinoma Using Network Pharmacology and Weighted Gene Co-Expression Network." Journal of Immunology Research 2020 (May 20, 2020): 1–17. http://dx.doi.org/10.1155/2020/7503605.
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The study aimed to clarify the potential immune-related targets and mechanisms of Qingyihuaji Formula (QYHJ) against pancreatic cancer (PC) through network pharmacology and weighted gene co-expression network analysis (WGCNA). Active ingredients of herbs in QYHJ were identified by the TCMSP database. Then, the putative targets of active ingredients were predicted with SwissTargetPrediction and the STITCH databases. The expression profiles of GSE32676 were downloaded from the GEO database. WGCNA was used to identify the co-expression modules. Besides, the putative targets, immune-related targets, and the critical module genes were mapped with the specific disease to select the overlapped genes (OGEs). Functional enrichment analysis of putative targets and OGEs was conducted. The overall survival (OS) analysis of OGEs was investigated using the Kaplan-Meier plotter. The relative expression and methylation levels of OGEs were detected in UALCAN, human protein atlas (HPA), Oncomine, DiseaseMeth version 2.0 and, MEXPRESS database, respectively. Gene set enrichment analysis (GSEA) was conducted to elucidate the key pathways of highly-expressed OGEs further. OS analyses found that 12 up-regulated OGEs, including CDK1, PLD1, MET, F2RL1, XDH, NEK2, TOP2A, NQO1, CCND1, PTK6, CTSE, and ERBB2 that could be utilized as potential diagnostic indicators for PC. Further, methylation analyses suggested that the abnormal up-regulation of these OGEs probably resulted from hypomethylation, and GSEA revealed the genes markedly related to cell cycle and proliferation of PC. This study identified CDK1, PLD1, MET, F2RL1, XDH, NEK2, TOP2A, NQO1, CCND1, PTK6, CTSE, and ERBB2 might be used as reliable immune-related biomarkers for prognosis of PC, which may be essential immunotherapies targets of QYHJ.
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Qin, Sha, Gaoming Liu, Haoer Jin, Xue Chen, Jiang He, Juxiong Xiao, Yan Qin, Yitao Mao, and Luqing Zhao. "The Dysregulation of SOX Family Correlates with DNA Methylation and Immune Microenvironment Characteristics to Predict Prognosis in Hepatocellular Carcinoma." Disease Markers 2022 (April 13, 2022): 1–21. http://dx.doi.org/10.1155/2022/2676114.
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Background. Due to the molecular heterogeneity of hepatocellular carcinoma (HCC), majority of patients respond poorly among various of therapy. This study is aimed at conducting a comprehensive analysis about roles of SOX family in HCC for obtaining more therapeutic targets and biomarkers which may bring new ideas for the treatment of HCC. Methods. UALCAN, Kaplan Meier plotter, cBioPortal, STRING, WebGestalt, Metascape, TIMER 2.0, DiseaseMeth, MethSurv, HPA, CCLE database, and Cytoscape software were used to comprehensively analyze the bioinformatic data. Results. SOX2, SOX4, SOX8, SOX10, SOX11, SOX12, SOX17, and SOX18 were significantly differentially expressed in HCC and normal tissues and were valuable for the grade and survival of HCC patients. In addition, the gene alterations of SOX family happened frequently, and SOX4 and SOX17 had the highest mutation rate. The function of SOX family on HCC may be closely correlated with the regulation of angiogenesis-related signaling pathways. Moreover, SOX4, SOX8, SOX11, SOX12, SOX17, and SOX18 were correlation with 8 types of immune cells (including CD8+ T cell, CD4+ T cell, B cell, Tregs, neutrophil, macrophage, myeloid DC, and NK cell), and we found that most types of immune cells had a positive correlation with SOX family. Notably, CD4+ T cell and macrophage were positively related with all these SOX family. NK cells were negatively related with most SOX family genes. DNA methylation levels in promoter area of SOX2, SOX4, and SOX10 were lower in HCC than normal tissues, while SOX8, SOX11, SOX17, and SOX18 had higher DNA methylation levels than normal tissues. Moreover, higher DNA methylation level of SOX12 and SOX18 demonstrated worse survival rates in patients with HCC. Conclusion. SOX family genes could predict the prognosis of HCC. In addition, the regulation of angiogenesis-related signaling pathways may participate in the development of HCC. DNA methylation level and immune microenvironment characteristics (especially CD4+ T cell and macrophage immune cell infiltration) could be a novel insight for predicting prognosis in HCC.
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Peng, Lu-Shan, Sai-Li Duan, Run-Qi Li, Zi-Yuan Bai, Chun-Lin Ou, and Jun-Pu Wang. "Prognostic value of sirtuin family members and experimental verification identify SIRT5 as diagnostic biomarkers in clear cell renal cell carcinoma." PeerJ 11 (April 19, 2023): e15154. http://dx.doi.org/10.7717/peerj.15154.
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Background The sirtuins (SIRTs) family is a nicotinamide adenine dinucleotide (NAD+) family of dependent deacetylases, which includes SIRT1-7. This family is related to the development and progression of various tumors. However, a comprehensive analysis of the role of SIRTs in clear cell renal cell carcinoma (ccRCC) is still lacking, and there are few reports on the inhibitory role of SIRT5 in ccRCC. Methods We used immunohistochemical analysis, and several bioinformatic databases to perform an integrated analysis of the expression and prognostic value of SIRT5 and other SIRT family members in ccRCC along with the associated immune cell infiltration. These databases include TIMER, THPA, cell culture, UALCAN, cBioPortal, WebGestalt, Metascape, DiseaseMeth, STRING database, and Cytoscape. Results The protein expression of SIRT1, 2, 3, 6, and 7 were upregulated in ccRCC for the Human Protein Atlas database, whereas the expression of SIRT4 and SIRT5 was decreased. The expression based on tumor stage, and grade followed a similar trend. Kaplan–Meier analysis showed that high SIRT4 and SIRT5 expression was positively related to better overall survival (OS), whereas SIRT6 and SIRT7 expression was positively related to worse OS. Further, high SIRT3 expression was related to worse relapse-free survival (RFS), whereas high SIRT5 expression was related to better RFS. To explore the mechanism underlying the function of SIRTs in ccRCC, we also used several databases to perform the functional enrichment analysis and explore the relationship between infiltrating immune cells and seven SIRT family members in ccRCC. The results showed that several SIRT family members, and particularly SIRT5, are correlated with the infiltration of some important immune cells. The protein expression of SIRT5 was significantly lower in tumor tissue compared to normal tissue and was negatively related to the age of the patient ccRCC individual tumor stages, and grades. In human ccRCC samples, strong IHC staining expression of SIRT5 was displayed in adjacent normal tissue than in tumor tissues. Conclusion SIRT5 may be a prognostic marker and a novel strategy for the treatment of ccRCC.
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Marques, Vastí Ferrari, Cícera Aparecida Escoura Bueno, Cleane Aparecida dos Santos, Eliane Reame, and Marjorie Samira Ferreira Bolognani. "SCHOOL DISEASEMENT: A PATHWAY OF THE MUNICIPAL EDUCATION SYSTEM OF JUNDIAÍ." International Journal of Human Sciences Research 2, no. 10 (April 18, 2022): 2–7. http://dx.doi.org/10.22533/at.ed.5582102214045.
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Stepanyan, Suren, V. M. Hakobyan, A. A. Petrosyan, H. H. Yeghiazaryan, K. T. Papazyan, H. Kh Batikyan, A. Yu Aleksanyan, H. H. Safaryan, H. H. Shmavonyan, and A. M. Babayan. "Complete versus non-complete fundoplication in surgical treatment of gastroesophageal reflux disease." NEW ARMENIAN MEDICAL JOURNAL, no. 4 (2022): 64–73. http://dx.doi.org/10.56936/18290825-2022.16.4-64.
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Gastroesophageal reflux disease is a common disorder accounting for approximately 75% of esophageal pathology. It seriously compromises quality of life. It develops when the reflux of gastric content causes troublesome symptoms or complications. During the last decades significant changes have occured in the role of surgery for gastroesophageal reflux disease. Initially antireflux surgery was reserved only for patients who had failed any kind of medical therapy. Now the range of indications for antireflux procedures is wide. Operations for gastroesophageal reflux disease are now well established and have good short- and long-term results, but no unique laparoscopic antireflux technique has been accepted so far, and a number of different antireflux procedures with numerous modifications have been reported. A total of 102 consecutive patients with gastroesophageal reflux disease were operated in the clinic of Republican Medical Center ‘’Armenia’’ (Yerevan, Armenia) and Mickaelyan Institute of Surgery (Yerevan, Armenia) from 2010 to 2021. In all cases the esophagogram showed hiatal hernia. Nissen, Nissen-Rossetti and Toupet fundoplications were performed as antireflux procedures. In all cases of combination of hiatal hernia and Gastroesophageal reflux diseasemesh reinforcement was performed. The results of follow-up assessment of the operated patients were compared. The results in early postoperative period were assessed with contrast X-ray examination and 24-hour pH-metry on the 5-th to 7-th days after surgery. The quality-of-life evaluation by the questionnaire showed a significant difference between the two groups, improvement of results in the laparoscopy group with complete fundoplication in comparison with not complete fundoplication. Complete fundoplication is a more reliable method of antireflux procedures for surgical treatment of gastroesophageal reflux disease. The division of short gastric vessels helps to prevent persistent dysphagia. The repair of esophageal hiatus of diaphragm is mandatory in antireflux procedures.
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Peng, Lu-Shan, Sai-Li Duan, Run-Qi Li, Dan Wang, Ying-Ying Han, Tao Huang, Yu-Pei Yu, Chun-Lin Ou, and Jun-Pu Wang. "Prognostic value and immune infiltration of the gasdermin family in lung adenocarcinoma." Frontiers in Oncology 12 (November 25, 2022). http://dx.doi.org/10.3389/fonc.2022.1043862.
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BackgroundThe GSDM family includes six members, GSDMA, GSDMB, GSDMC, GSDMD, GSDME (DFNA5), and PJVK (Pejvakin, DFNB59), which can induce pyroptosis, thereby regulating the tumorigenesis of various cancers. However, the clinical characteristics and role of the GSDM family in LUAD are not well understood.MethodsIn this study, several important bioinformatics databases were used to integrate the analysis of the expression, prognostic value, and immune infiltration of GSDMs in LUAD. These databases include UALCAN, DiseaseMeth, GEPIA, THPA, cBioPortal, TIMER, WebGestalt, STRING database, and Cytoscape.ResultsThe findings from the UALCAN database revealed that the expression of all six GSDMs based on the tumor stage in LUAD was increased (particularly GSDMD). Our IHC results verified it. Additionally, the DiseaseMeth database showed that the methylation levels of GSDMA, GSDMB, GSDMC, and GSDMD were decreased. The expression of six GSDMs was related to shorter overall survival in patients with LUAD, according to the GEPIA database. The cBioPortal database was further used to explore the alteration rate and correlated genes in LUAD. Subsequently, these genes were subjected to functional enrichment and protein-protein interaction network analyses. We identified that the GSDM family regulate several signaling pathways, including immune-associated signaling pathways. According to tumor-infiltrating immune cell analysis from the TIMER database, GSDM family members are associated with the infiltration of important immune cells and their signature markers.ConclusionsGSDM family may be prognostic markers and novel strategies for the treatment of LUAD.
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Fan, Yu, Lijia He, Yu Wang, Shaozhi Fu, Yunwei Han, Juan Fan, and Qinglian Wen. "CLIP4 Shows Putative Tumor Suppressor Characteristics in Breast Cancer: An Integrated Analysis." Frontiers in Molecular Biosciences 7 (January 26, 2021). http://dx.doi.org/10.3389/fmolb.2020.616190.
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Background: CAP-Gly domain containing linker protein family member 4 (CLIP4) plays an important role in cancers. However, its expression, prognostic value, and biological effect in breast cancer remain unclear.Methods: Data on patients diagnosed with breast cancer were retrieved from the TCGA-BRCA and other public omics databases. The expression profile of CLIP4 was analyzed using Oncomine, bc-GenExMiner, and TCGA. The prognostic value of CLIP4 was determined by Kaplan-Meier Plotter and Human Protein Atlas. Identification of genes co-expressed with CLIP4 and potential mechanism analyses were performed using UALCAN, STRING, Metascape, and GSEA. The epigenetic characteristics of CLIP4 were determined by DiseaseMeth and MEXPRESS.Results: CLIP4 was downregulated and its expression was negatively correlated with estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor type 2 (HER2) status, Nottingham prognostic index (NPI), and Scarff-Bloom-Richardson (SBR) grade in breast cancer, whereas it was positively linked to basal-like and triple negative breast cancer status. Ectopic expression of CLIP4 was related with poor prognosis. In the analysis of genes co-expressed with CLIP4, GSEA showed that the Hedgehog (Hh), JAK-STAT, ERBB, Wnt signaling pathway, cell adhesion molecules, and pathways in cancer were dissimilarly enriched in the CLIP4 expression high phenotype. Analysis of the genetics and epigenetics of CLIP4 indicated that its expression was negatively correlated with DNA methylation.Conclusion: Methylated CLIP4 may be a novel prognostic and therapeutic biomarker for breast cancer.
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Wu, Geting, Yuanliang Yan, Yuan Cai, Bi Peng, Juanni Li, Jinzhou Huang, Zhijie Xu, and Jianhua Zhou. "ALKBH1-8 and FTO: Potential Therapeutic Targets and Prognostic Biomarkers in Lung Adenocarcinoma Pathogenesis." Frontiers in Cell and Developmental Biology 9 (June 3, 2021). http://dx.doi.org/10.3389/fcell.2021.633927.
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The AlkB family consists of Fe(II)- and α-ketoglutarate-dependent dioxygenases that can catalyze demethylation on a variety of substrates, such as RNA and DNA, subsequently affecting tumor progression and prognosis. However, their detailed functional roles in lung adenocarcinoma (LUAD) have not been clarified in a comprehensive manner. In this study, several bioinformatics databases, such as ONCOMINE, TIMER, and DiseaseMeth, were used to evaluate the expression profiles and prognostic significance of the AlkB family (ALKBH1-8 and FTO) in LUAD. The expression levels of ALKBH1/2/4/5/7/8 were significantly increased in LUAD tissues, while the expression levels of ALKBH3/6 and FTO were decreased. The main functions of differentially expressed AlkB homologs are related to the hematopoietic system and cell adhesion molecules. We also found that the expression profiles of the AlkB family are highly correlated with infiltrating immune cells (i.e., B cells, CD8 + T cells, CD4 + T cells, macrophages, neutrophils and dendritic cells). In addition, DNA methylation analysis indicated that the global methylation levels of ALKBH1/2/4/5/6/8 and FTO were decreased, while the global methylation levels of ALKBH3/7 were increased. In addition, the patients with upregulated ALKBH2 have significantly poor overall survival (OS) and post-progressive survival (PPS). Taken together, our work could provide insightful information about aberrant AlkB family members as potential biomarkers for the diagnostic and prognostic evaluation of LUAD. Especially, ALKBH2 could be served as a therapeutic candidate for treating LUAD.
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Fang, Qinghua, Tingyue Li, Peiya Chen, Yuzhe Wu, Tingting Wang, Lixia Mo, Jiaxin Ou, and Kutty Selva Nandakumar. "Comparative Analysis on Abnormal Methylome of Differentially Expressed Genes and Disease Pathways in the Immune Cells of RA and SLE." Frontiers in Immunology 12 (May 17, 2021). http://dx.doi.org/10.3389/fimmu.2021.668007.
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We identified abnormally methylated, differentially expressed genes (DEGs) and pathogenic mechanisms in different immune cells of RA and SLE by comprehensive bioinformatics analysis. Six microarray data sets of each immune cell (CD19+ B cells, CD4+ T cells and CD14+ monocytes) were integrated to screen DEGs and differentially methylated genes by using R package “limma.” Gene ontology annotations and KEGG analysis of aberrant methylome of DEGs were done using DAVID online database. Protein-protein interaction (PPI) network was generated to detect the hub genes and their methylation levels were compared using DiseaseMeth 2.0 database. Aberrantly methylated DEGs in CD19+ B cells (173 and 180), CD4+ T cells (184 and 417) and CD14+ monocytes (193 and 392) of RA and SLE patients were identified. We detected 30 hub genes in different immune cells of RA and SLE and confirmed their expression using FACS sorted immune cells by qPCR. Among them, 12 genes (BPTF, PHC2, JUN, KRAS, PTEN, FGFR2, ALB, SERB-1, SKP2, TUBA1A, IMP3, and SMAD4) of RA and 12 genes (OAS1, RSAD2, OASL, IFIT3, OAS2, IFIH1, CENPE, TOP2A, PBK, KIF11, IFIT1, and ISG15) of SLE are proposed as potential biomarker genes based on receiver operating curve analysis. Our study suggests that MAPK signaling pathway could potentially differentiate the mechanisms affecting T- and B- cells in RA, whereas PI3K pathway may be used for exploring common disease pathways between RA and SLE. Compared to individual data analyses, more dependable and precise filtering of results can be achieved by integrating several relevant data sets.
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Sun, Zhuolun, Yunhua Mao, Xu Zhang, Shuo Lu, Hua Wang, Chi Zhang, Chutian Xiao, et al. "Identification of ARHGEF38, NETO2, GOLM1, and SAPCD2 Associated With Prostate Cancer Progression by Bioinformatic Analysis and Experimental Validation." Frontiers in Cell and Developmental Biology 9 (September 1, 2021). http://dx.doi.org/10.3389/fcell.2021.718638.
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Prostate cancer (PCa) represents one of the most prevalent types of cancers and is a large health burden for men. The pathogenic mechanisms of PCa still need further investigation. The aim of this study was to construct an effective signature to predict the prognosis of PCa patients and identify the biofunctions of signature-related genes. First, we screened differentially expressed genes (DEGs) between PCa and normal control tissues in The Cancer Genome Atlas (TCGA) and GSE46602 datasets, and we performed weighted gene co-expression network analysis (WGCNA) to determine gene modules correlated with tumors. In total, 124 differentially co-expressed genes were retained. Additionally, five genes (ARHGEF38, NETO2, PRSS21, GOLM1, and SAPCD2) were identified to develop the prognostic signature based on TCGA dataset. The five-gene risk score was verified as an independent prognostic indicator through multivariate Cox regression analyses. The expression of the five genes involved in the signature was detected in the Gene Expression Omnibus (GEO), Gene Expression Profiling Interactive Analysis (GEPIA), and Oncomine databases. In addition, we utilized DiseaseMeth 2.0 and MEXPRESS for further analysis and found that abnormal methylation patterns may be a potential mechanism for these five DEGs in PCa. Finally, we observed that these genes, except PRSS21, were highly expressed in tumor samples and PCa cells. Functional experiments revealed that silencing ARHGEF38, NETO2, GOLM1, and SAPCD2 suppressed the proliferation, migration, and invasiveness of PCa cells. In summary, this prognostic signature had significant clinical significance for treatment planning and prognostic evaluation of patients with PCa. Thus, ARHGEF38, NETO2, GOLM1, and SAPCD2 may serve as oncogenes in PCa.
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Zhang, Ziying, Peng Chen, Hui Xie, and Peiguo Cao. "Overexpression of GINS4 Is Associated With Tumor Progression and Poor Survival in Hepatocellular Carcinoma." Frontiers in Oncology 11 (March 25, 2021). http://dx.doi.org/10.3389/fonc.2021.654185.
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PurposeOur research was aimed to identify the expression, clinical value and biological significance of GINS complex subunit 4 (GINS4) in hepatocellular carcinoma (HCC).Materials and MethodsGINS4 was initially screened through weighted gene co-expression network analysis (WGCNA). The TCGA, GEO, and TIMER databases were applied for analyzing the GINS4 mRNA expression in HCC. GINS4 protein levels were detected via immunohistochemistry (IHC). Receiver operating characteristic (ROC) curve was applied for estimating the diagnostic significance of GINS4 in HCC. Kaplan-Meier plots, Cox model, and nomogram were used to assess the prognostic performance of GINS4 in HCC. Nomogram validation was conducted through time-dependent ROC and decision curve analysis (DCA). The Wanderer, UALCAN, and DiseaseMeth databases were utilized to identify GINS4 methylation levels in HCC. Genes co-expressed with GINS4 in HCC were estimated through the TCGA, cBioPortal, and GEPIA. GO, KEGG, and GSEA unraveled the possible biological mechanisms of GINS4 in HCC.ResultsWGCNA confirmed that GINS4 was one of hub genes significantly associated with histological grade of HCC. Multiple databases confirmed the significant upregulation of GINS4 in HCC tissues compared with non-tumor controls. IHC analysis of 35 HCC patients demonstrated that overexpressed GINS4 positively correlated with advanced TNM stage and poor pathological differentiation. GINS4 could effectively differentiate HCC cases from healthy individuals, with an AUC of 0.865. Increased GINS4 expression predicted unsatisfactory prognosis in HCC patients, especially in age >60 years, histological grade 1, HBV infection-negative, and occurring relapse subgroup. Nomogram incorporating GINS4 level and TNM stage displayed satisfactory predictive accuracy and clinical utility in predicting HCC prognosis. Upregulated GINS4 exhibited hypomethylated levels in HCC. Functional analysis indicated that GINS4 potentially positively modulated cell cycle and PI3K/AKT/mTOR pathway.ConclusionGINS4 is overexpressed in HCC and is correlated with undesirable survival of HCC patients.
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Hu, Xiaoyi, Mingyang Bao, Jiacheng Huang, Lin Zhou, and Shusen Zheng. "Identification and Validation of Novel Biomarkers for Diagnosis and Prognosis of Hepatocellular Carcinoma." Frontiers in Oncology 10 (September 25, 2020). http://dx.doi.org/10.3389/fonc.2020.541479.
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Introduction: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide due to poor survival outcome. Thus, there is an urgent need to identify effective biomarkers for early diagnosis and prognosis prediction.Methods: A total of 389 differentially expressed genes (DEGs) between HCC samples and normal were selected based on the Robust Rank Aggregation (RRA) method. We combined DEGs expression and clinical traits to construct a gene co-expression network through WGCNA. Forty hub genes were selected from the key module. Among them, YWHAB, PPAT, NOL10 were eventually identified as prognostic biomarkers using multivariate Cox regression model. Biomarkers expression pattern was investigated by informatic analysis and verified by RNA-seq of 32 patients with HCC. DiseaseMeth 2.0, MEXPRESS, and Tumor Immune Estimation Resource (TIMER) were used to assess the methylation and immune status of biomarkers. GSVA, CCK8, colony formation assay, Edu imaging kit, wound-healing assay, and xenograft tumor model were utilized to investigate the effects of biomarkers on proliferation, metastasis of HCC cells in vitro, and in vivo. The Kaplan–Meier (KM) plotter and ROC curves were used to validate the prognostic and diagnostic value of biomarker expression.Results: All the selected biomarkers were upregulated in HCC samples and higher expression levels were associated with advanced tumor stages and T grades. The regulation of YWHAB, PPAT, NOL10 promoter methylation varied in tumors, and precancerous normal tissues. Immune infiltration analysis suggested that the abnormal regulations of these biomarkers were likely attributed to B cells and dendritic cells. GSVA for these biomarkers showed their great contributions to proliferation of HCC. Specific inhibition of their expression had strong effects on tumorigenesis in vitro and in vivo. ROC and KM curves confirmed their usefulness of diagnosis and prognosis of HCC.Conclusions: These findings identified YWHAB, PPAT, and NOL10 as novel biomarkers and validated their diagnostic and prognostic value for HCC.
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Song, Liying, Rong Zeng, Keda Yang, Wei Liu, Zhijie Xu, and Fanhua Kang. "The biological significance of cuproptosis-key gene MTF1 in pan-cancer and its inhibitory effects on ROS-mediated cell death of liver hepatocellular carcinoma." Discover Oncology 14, no. 1 (June 28, 2023). http://dx.doi.org/10.1007/s12672-023-00738-8.
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AbstractMetal regulatory transcription factor 1 (MTF1) has been reported to be correlated with several human diseases, especially like cancers. Exploring the underlying mechanisms and biological functions of MTF1 could provide novel strategies for clinical diagnosis and therapy of cancers. In this study, we conducted the comprehensive analysis to evaluate the profiles of MTF1 in pan-cancer. For example, TIMER2.0, TNMplot and GEPIA2.0 were employed to analyze the expression values of MTF1 in pan-cancer. The methylation levels of MTF1 were evaluated via UALCAN and DiseaseMeth version 2.0 databases. The mutation profiles of MTF1 in pan-cancers were analyzed using cBioPortal. GEPIA2.0, Kaplan–Meier plotter and cBioPortal were also used to explore the roles of MTF1 in cancer prognosis. We found that high MTF1 expression was related to poor prognosis of liver hepatocellular carcinoma (LIHC) and brain lower grade glioma (LGG). Also, high expression level of MTF1 was associated with good prognosis of kidney renal clear cell carcinoma (KIRC), lung cancer, ovarian cancer and breast cancer. We investigated the genetic alteration and methylation levels of MTF1 between the primary tumor and normal tissues. The relationship between MTF1 expression and several immune cells was analyzed, including T cell CD8 + and dendritic cells (DC). Mechanically, MTF1-interacted molecules might participate in the regulation of metabolism-related pathways, such as peptidyl-serine phosphorylation, negative regulation of cellular amide metabolic process and peptidyl-threonine phosphorylation. Single cell sequencing indicated that MTF1 was associated with angiogenesis, DNA repair and cell invasion. In addition, in vitro experiment indicated knockdown of MTF1 resulted in the suppressed cell proliferation, increased reactive oxygen species (ROS) and promoted cell death in LIHC cells HepG2 and Huh7. Taken together, this pan-cancer analysis of MTF1 has implicated that MTF1 could play an essential role in the progression of various human cancers.
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Wang, Yongkang, Yinfeng Yang, Honglei Gao, Ting Ouyang, Luyao Zhang, Jili Hu, Sheng Hu, and Hongxing Kan. "Comprehensive Analysis of CDCAs Methylation and Immune Infiltrates in Hepatocellular Carcinoma." Frontiers in Oncology 10 (February 16, 2021). http://dx.doi.org/10.3389/fonc.2020.566183.
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BackgroundAs essential components of cycle growth, the cell division cycle-associated family genes (CDCAs) have crucial roles in tumor development and progression, especially in hepatocellular carcinoma (HCC). However, due to the tumor heterogeneity of HCC, little is known about the methylation variability of CDCAs in mediating phenotypic changes (e.g., immune infiltrates) in HCC. Presently, we aim to comprehensively explore the expression and prognosis of CDCAs methylation with regard to immune infiltrates of HCC.MethodsWe first identified the correlating differentially expressed genes (co-DEGs) among 19 different types of cancer cohorts (a total of 7,783 patients) and then constructed the weighted gene co-expressed and co-methylated networks. Applying the clustering analysis, significant modules of DEGs including CDCAs were selected and their functional bioinformatics analyses were performed. Besides, using DiseaseMeth and TIMER, the correlation between the methylation levels of CDCAs and tumor immune infiltrates was also analyzed. In final, to assess the influence of CDCAs methylation on clinical prognosis, Kaplan-Meier and Cox regression analysis were carried out.ResultA total of 473 co-DEGs are successfully identified, while seven genes of CDCAs (CDCA1–3 and CDCA5–8) have significant over-expression in HCC. Co-expressed and co-methylated networks reveal the strong positive correlations in mRNA expression and methylation levels of CDCAs. Besides, the biological enrichment analysis of CDCAs demonstrates that they are significantly related to the immune function regulation of infiltrating immune cells in HCC. Also, the methylation analysis of CDCAs depicts the strong association with the tumor immunogenicity, i.e., low-methylation of CDCA1, CDCA2, and CDCA8 dramatically reduced the immune infiltrate levels of T cells and cytotoxic lymphocytes. Additionally, CDCA1–6 and CDCA8 with low-methylation levels significantly deteriorate the overall survival of patients in HCC.ConclusionsThe co-expressed and co-methylated gene networks of CDCAs show a powerful association with immune function regulation. And the methylation levels of CDCAs suggesting the prognostic value and infiltrating immune differences could be a novel and predictive biomarker for the response of immunotherapy.
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Wang, Jinxiang, Jie Jin, Yanling Liang, Yihe Zhang, Nisha Wu, Mingming Fan, Fangyin Zeng, and Fan Deng. "miR-21-5p/PRKCE axis implicated in immune infiltration and poor prognosis of kidney renal clear cell carcinoma." Frontiers in Genetics 13 (September 13, 2022). http://dx.doi.org/10.3389/fgene.2022.978840.
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Kidney renal clear cell carcinoma (KIRC or ccRCC) is the most notorious subtype of renal cell carcinoma for its poor prognosis. Mounting evidence has highlighted the key role of PRKCE in the initiation and development of several types of human cancer, including kidney renal clear cell carcinoma (KIRC). However, the mechanism of PRKCE aberrant expression and the specific clinical correlation of PRKCE expression with immune cell infiltration in KIRC remains elusive. Therefore, we analyzed the relationship between PRKCE and KIRC using many databases, including Oncomine, TCGA, GTEx, TIMER, and GEO. We found that PRKCE decreased in KIRC tumor tissue compared to normal tissue. The Kaplan-Meier Plotter analysis and Univariate and Multivariate Cox analyses were used to evaluate the association between PRKCE and clinicopathological variables and prognosis. Low PRKCE expression was associated with poor survival and histologic grade, T stage, pathologic stage, and M stage. Besides, the C-indexes and calibration plots of the nomogram based on multivariate analysis showed an effective predictive performance for KIRC patients. In addition, PRKCE may be positively correlated with inflammation and negatively correlated with proliferation, metastasis, and invasion as identified by CancerSEA. Moreover, overexpression of PRKCE suppressed ACHN and Caki-1 cell proliferation, migration, and invasion in vitro. Additionally, methylation level data acquired from UALCAN, DiseaseMeth, CCLE, LinkedOmics, and MEXPRESS was used to investigate the relationship between PRKCE expression and PRKCE methylation level. Furthermore, upstream potential miRNA predictions were further performed to explore the mechanism of PRKCE decreased expression in KIRC using multiple online databases available on publicly assessable bioinformatics platforms. High PRKCE methylation levels and hsa-miR-21-5p may contribute to PRKCE low expression in KIRC. Finally, an analysis of immune infiltration indicated that PRKCE was associated with immune cell infiltration. Importantly, PRKCE may affect prognosis partially by regulating immune infiltration in KIRC. In summary, PRKCE may serve as a novel prognostic biomarker reflecting immune infiltration level and a novel therapeutic target in KIRC.
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Zhao, Shijian, Yinteng Wu, Yantao Wei, Xiaoyu Xu, and Jialin Zheng. "Identification of Biomarkers Associated With CD8+ T Cells in Coronary Artery Disease and Their Pan-Cancer Analysis." Frontiers in Immunology 13 (June 21, 2022). http://dx.doi.org/10.3389/fimmu.2022.876616.
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PurposeTo identify biomarkers associated with CD8+ T cells in coronary artery disease (CAD) and initially explore their potential role in the tumor immune microenvironment.Materials and MethodsCAD-related datasets GSE12288, GSE34198, and GSE66360, were downloaded from the GEO database. First, GSVA was performed based on the GSE12288 dataset. Then WGCNA analysis was performed to identify the most relevant module and candidate hub gene for CD8+ T cells, followed by GO and KEGG analysis of this module. Secondly, the relationship between candidate hub genes and CD8+ T cells was verified using GSE34198 and GSE66360, which led to the identification of hub genes. The relationship of hub genes with CD8+ T cells in cancer was analyzed using the TIMER database. Methylation analysis of hub genes was performed using the DiseaseMeth database. CAD, pan-cancer, pan-cell lines, and pan-normal tissues, correlations between hub genes. In addition, potential drugs and TFs associated with hub genes were predicted, and the ceRNA network was constructed. Finally, GSEA was performed separately for hub genes.ResultsCAD was shown to be associated with immune response by GSVA analysis. WGCNA identified the blue module as most related to CD8+ T cells and identified nine candidate hub genes. The relevance of CAD to immunity was further confirmed by GO and KEGG analysis of the module. Two additional datasets validated and identified three hub genes (FBXO7, RAD23A, and MKRN1) that significantly correlated with CD8+ T cells. In addition, we found that hub genes were positively associated with CD8+ T cells in TGCT, THCA, and KICH cancers by our analysis. Moreover, the hub gene was differentially methylated. We also analyzed the correlation between hub genes in CAD, different cancers, different cell lines, and different normal tissues. The results of all the analyses showed a positive correlation between them. Finally, we successfully constructed hub gene-associated TF-gene and ceRNA networks and predicted 11 drugs associated with hub genes. GSEA suggests that hub genes are related to multiple immune response processes.ConclusionFBXO7, RAD23A, and MKRN1 are significantly associated with CD8+ T cells in CAD and multiple cancers and may act through immune responses in CAD and cancer.
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Wang, Yumian, Li Zhang, Han Chen, Juan Yang, Yun Cui, and Hong Wang. "Coronary artery disease-associated immune gene RBP1 and its pan-cancer analysis." Frontiers in Cardiovascular Medicine 10 (March 9, 2023). http://dx.doi.org/10.3389/fcvm.2023.1091950.
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PurposeTo identify immune-related biomarkers in coronary artery disease (CAD), investigate their possible function in the immunological milieu of tumors, and initially investigate the mechanisms and therapeutic targets shared by CAD and cancer.MethodsDownload the CAD-related dataset GSE60681 from the GEO database. GSVA and WGCNA analyses were performed based on the GSE60681 dataset to identify the modules most pertinent to CAD, identify candidate hub genes and finally intersect the genes associated with immunity downloaded from the import database to find the hub genes. The GTEx, CCLE, and TCGA database were used to examine the expression of the hub gene in normal tissues, tumor cell lines, tumor tissues, and different tumor STAGES. One-factor cox and Kaplan-Meier analyses were performed to explore the prognosis of hub genes. Hub gene methylation levels in CAD and cancer were analyzed in the diseaseMeth 3.0 and ualcan databases, respectively. R package CiberSort processed the GSE60681 dataset to assess immune infiltration in CAD. TIMER2.0 evaluated hub genes with pan-cancer immune infiltration. The hub genes were analyzed for drug sensitivity and correlation with TMB, MSI, MMR, cancer-related functional status, and immune checkpoints in different tumors. Finally, GSEA was carried out on the crucial genes.ResultsWGCNA were used to pinpoint the green modules that were most closely related to CAD and intersections with immune-related genes were taken to remember the pivotal gene RBP1. RBP1 is hypermethylated in CAD and multiple cancers. Its expression levels in different cancers were associated with poor prognosis of cancer, with significant expression levels at higher stages of cancer staging. The immune infiltration results showed that RBP1 was closely associated with CAD and tumor-associated immune infiltration. The results indicated that RBP1 was strongly correlated with TMB, MSI, MMR, cancer-associated functional status, and immune checkpoints in various cancers. RBP1 was related to the sensitivity of six anticancer drugs. GSEA showed RBP1 was associated with immune cell activation, immune response, and cancer development.ConclusionRBP1 is a pivotal gene associated with immunity in CAD and pan-cancer and may mediate the development of CAD and cancer through immunity, making it a common therapeutic target for both.