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در نشریات گروه پزشکی
  • Junhua Tian, Xiaochun Liu *
    Background

    Endometriosis is a chronic gynecological disorder characterized by the ectopic growth of endometrial tissue outside the uterus, leading to debilitating painandinfertility in affectedwomen. Despite its prevalenceandclinical significance, the molecularmechanismsunderlying the progression of endometriosisremainpoorly understood. This studyemploys bioinformatics toolsandmolecular docking simulations to unravel the intricate genetic and molecular networks associated with endometriosis progression.

    Objectives

    The primary objectives of this research are to identify differentially expressed genes (DEGs) linked to endometriosis, elucidate associated biological pathways using the Database for Annotation, Visualization, and Integrated Discovery (DAVID), construct a Protein-Protein Interaction (PPI) network to identify hub genes, and perform molecular docking simulations to explore potential ligand-protein interactions associated with endometriosis.

    Methods

    Microarray data from Homo sapiens, specifically Accession: GDS3092 Series = GSE5108 (Platform: GPL2895), were retrieved from the NCBI Gene Expression Omnibus (GEO). The data underwent rigorous preprocessing and DEG analysis using NCBI GEO2. Database for Annotation, Visualization, and Integrated Discovery analysis was employed for functional annotation, and a PPI network was constructed using the STITCH database and Cytoscape 3.8.2. Molecular docking simulations against target proteins associated with endometriosis were conducted using MVD 7.0.

    Results

    A total of 1 911 unique elements were identified as DEGs associated with endometriosis from the microarray data. Database for Annotation, Visualization, and Integrated Discovery analysis revealed pathways and biological characteristics positively and negatively correlated with endometriosis. Hubgenes, including BCL2, CCNA2, CDK7, EGF, GAS6, MAP3K7, and TAB2, were identified through PPI network analysis. Molecular docking simulations highlighted potential ligands, such as Quercetin-3-o-galactopyranoside and Kushenol E, exhibiting favorable interactions with target proteins associated with endometriosis.

    Conclusions

    This study provides insights into the molecular signatures, pathways, and hub genes associated with endometriosis. Utilizing DAVID in this study clarifies biological pathways associated with endometriosis, revealing insights into intricate genetic networks. Molecular docking simulations identified ligands for further exploration in therapeutic interventions. The consistent efficacy of these ligands across diverse targets suggests broad-spectrum effectiveness, encouraging further exploration for potential therapeutic interventions. The study contributes to a deeper understanding of endometriosis pathogenesis, paving the way for targeted therapies and precision medicine approaches to improve patient outcomes. These findings advance our understanding of the molecular mechanisms in endometriosis (EMS), offering promising avenues for future research and therapeutic development in addressing this complex condition.

    Keywords: Endometriosis, Microarray, Hub Genes, Molecular Docking, Bioinformatics Analysis
  • مالتیپل اسکلروزیس و مسیر سیگنال دهی MAPK : یک مطالعه مبتنی بر ریزآرایه
    میرزا علی مفضل جهرمی، امیر رضا دهقان، اباذر روستازاده*
    مقدمه

    بیماری مالتیپل اسکلروزیس (MS) یک بیماری التهابی دمیلینه کننده ی سیستم اعصاب مرکزی است. هدف از مطالعه ی کنونی بررسی کتابخانه های ریز آرایه موجود در NCBI و آنالیز عملکرد کتابخانه برای بررسی ژن های تغییربیان یافته و استخراج مسیرهای سلولی درگیر در پاتوژنز MS بود.

    روش کار

    داده های موجود در مجموعه داده GSE21942 ، در ابتدا توسط GEO2R و سپس توسط نرم افزار R نسخه 4.2.0 آنالیز شدند. نرمال سازی داده ها و استخراج ژن های دارای تفاوت بیان معنادار (DEGs) انجام شد و آنالیز عملکرد توسط Enrichr و DAVID 6.8 انجام شد.

    یافته ها

    300 ژن در گروه MS با Log2FC>1 افزایش بیان و 205 ژن با Log2FC<-1 کاهش بیان داشتند. مسیر پیام دهی گیرنده سلول B و مسیر پیام دهی MAPK کیناز مهمترین مسیر استخراج شده است.

    نتیجه گیری

    مسیرهای استخراج شده برای ژن های تغییر بیان یافته با مسیر پیام دهی MAPK کیناز مرتبط می باشند که ممکن است طیف گسترده ای از فرآیندهای سلولی از جمله تکثیر، تمایز، آپوپتوز و پاسخ های استرس را در بیماری MS تنظیم کنند. لذا مسیر اشاره شده احتمالا بتوانند به عنوان اهدافی جهت درمان MS مورد استفاده قرار گیرد.

    کلید واژگان: آنالیز عملکرد، ریز آرایه، مالتیپل اسکلروزیس
    Multiple sclerosis and the MAPK signaling pathway: a microarray-based study
    Mirza Ali Mofazzal Jahromi, Amirreza Dehghan, Abazar Roustazadeh *
    Background

    Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system. The aim of the current study was to search microarray libraries and perform functional analysis on extracted genes to predict their role in the pathogenesis of MS.

    Materials and methods

    The data in the GSE21942 dataset were first analyzed by GEO2R and then by R software version 4.2.0. Normalization of data and extraction of genes with significant expression differences (DEGs) were performed and performance analysis was performed by Enrichr and DAVID 6.8.

    Results

    300 genes in the MS group had increased expression with Log2FC>1 and 205 genes had decreased expression with Log2FC<-1. The B cell receptor signaling pathway and the MAPK kinase signaling pathway were the most important pathways extracted.

    Conclusion

    The extracted pathways for the altered genes are related to the MAPK kinase signaling pathway, which may regulate a wide range of cellular processes including proliferation, differentiation, apoptosis, and stress responses in MS. Therefore, the indicated pathways could potentially be used as targets for MS therapy.

    Keywords: Multiple Sclerosis, Functional Enrichment Analysis, Microarray
  • مهدی کریمی، حمیدرضا مرتضوی، محسن علیپور، اباذر روستازاده*
    مقدمه

    سرطان آناپلاستیک تیروئید (ATC) شکل تمایز نیافته ای از سرطان تیروئید است که کشندگی بالایی دارد. هدف از مطالعه کنونی جستجو در کتابخانه های ریزآرایه موجود در مرکز ملی اطلاعات زیست فناوری (NCBI) و آنالیز عملکرد بر روی ژن-های استخراج شده بود تا نقش آن ها در پاتوژنز ATC پیش بینی گردد.

    روش کار

    داده های موجود در مجموعه داده GSE33630 ، در ابتدا توسط GEO2R و سپس توسط نرم افزار R نسخه 4.2.0 آنالیز شدند. نرمال سازی داده ها و استخراج ژن های دارای تفاوت بیان معنادار (DEGs) انجام شد و آنالیز عملکرد توسط Enrichr و DAVID 6.8 انجام گرفت.

    یافته ها

    آنالیزها نشان داد که 1705 ژن با log2FC>1 افزایش بیان و 2740 ژن با log2FC<-1 کاهش بیان داشتند. همچنین مسیر پیام دهی PI3k/Akt و فاکتورهای نسخه برداری IRF8، TCF4، CBEPB و JUND با ژن های افزایش بیان یافته مرتبط هستند.

    نتیجه گیری

    افزایش فعالیت مسیر پیام دهی PI3k-Akt و همچنین فاکتورهای نسخه برداری IRF8، TCF4، CBEPB و JUND در سلول های تیروئید احتمالا منجر به ایجاد یا پیشرفت سرطان ATC می گردد.

    کلید واژگان: آنالیز عملکرد، ریز آرایه، سرطان آناپلاستیک تیروئید
    Mahdi Karimi, Hamidreza Mortezavi, Mohsen Alipour, Abazar Roustazadeh *
    Background

    Anaplastic thyroid cancer (ATC) is an undifferentiated form of thyroid cancer that is highly lethal. The aim of the current study was to search the microarray libraries available in the National Center for Biotechnology Information (NCBI) and analyze the function of the extracted genes to predict their role in the pathogenesis of ATC.

    Materials and methods

    The data in the GSE33630 dataset were first analyzed by GEO2R and then by R software version 4.2.0. Normalization of data and extraction of genes with significant expression differences (DEGs) were performed and performance analysis was performed by Enrichr and DAVID 6.8.

    Results

    The analyzes showed that 1705 genes with log2FC>1 had increased expression and 2740 genes with log2FC<-1 had decreased expression. Also, the PI3k/Akt signaling pathway and the transcription factors IRF8, TCF4, CBEPB and JUND are related to the increased expressed genes.

    Conclusion

    Increased activity of PI3k-Akt signaling pathway as well as transcription factors IRF8, TCF4, CBEPB and JUND in thyroid cells probably leads to the development or progression of ATC cancer.

    Keywords: Anaplastic Thyroid Cancer, Functional Enrichment Analysis, Microarray
  • مجید کوثری، محمدرضا تقوا، اباذر روستازاده*
    مقدمه

    سرطان سینه از شایع ترین سرطان ها در میان زنان می باشد. از آنجائیکه ریز آرایه روشی جدید در تشخیص سرطان می باشد، در مطالعه کنونی کتابخانه ریز آرایه سلول های سرطان سینه رده MCF-7 پس از پرتودهی بررسی گردید تا الگوی بیان ژن و مسیرهای متابولیسمی مرتبط با آن پیش بینی شود.

    روش کار

    داده های ریز آرایه استخراج شده از مرکز ملی اطلاعات زیست فناوری (NCBI) مربوط به سلول های MCF-7 توسط GEO2R و نرم افزارR مورد تحلیل قرار گرفتند. سپس ژن هایی که افزایش و کاهش بیان داشتند استخراج و با استفاده از پایگا های داده DAVID و Enrichr تحلیل عملکرد در مورد آن ها انجام شد.

    یافته ها

    در این مطالعه پس از 48 ساعت پرتودهی 234 ژن با Log2FC>1 افزایش بیان و 146 ژن با Log2FC<-1 کاهش بیان داشتند (Adjusted p value <0.05). آنالیز KEGG بر روی ژن های دارای افزایش بیان نشان داد که این ژن ها با بیماری دیابت نوع 1 در ارتباط می باشند (P= 2.43E-04). ژن های استخراج شده در این مسیر شامل HLA-DRB5, HLA-DRB4, CPE, TNF, HLA-DRB1 و HLA-DM بودند (Adjusted p value <0.05). همچنین یافته ها نشان می دهد که ژن هایی که در جزایر لانگرهانس در خصوص دیابت نوع 1 دخالت دارند شامل CPE ، MHC-II و TNF-α می باشد.

    نتیجه گیری

    یافته های این مطالعه نشان داد افزایش زمان پرتودهی در سلول های سرطان سینه احتمالا با واسطه ژن های CPE ، MHC-II و TNF-α در جزایر لانگرهانس منجر به فعال شدن مسیرهای مربوط به بیماری دیابت نوع 1 می گردد.

    کلید واژگان: پرتودهی، تحلیل عملکرد، دیابت نوع 1، ریز آرایه، سرطان سینه
    Majid Kowsari, Mohammadreza Taghva, Abazar Roustazadeh *

    Breast cancer is one of the most common cancers among women. Since microarray is a new method in cancer diagnosis, in the current study, the microarray library of MCF-7 breast cancer cells after irradiation was examined to predict the gene expression pattern and metabolic pathways related to it.Materials and Methods Microarray data extracted from National Center for Biotechnology Information (NCBI) related to MCF-7 cells were analyzed by GEO2R and R software. Then the genes that had increased and decreased expression were extracted and gene ontology analysis was performed using DAVID and Enrichr databases.

    Results

    In this study, after 48 hours of irradiation, 234 genes with Log2FC>1 increased expression and 146 genes with Log2FC<-1 decreased expression (Adjusted p value <0.05). KEGG analysis on genes with increased expression showed that these genes are related to type 1 diabetes (P=2.43E-04). The genes extracted in this pathway included HLA-DRB5, HLA-DRB4, CPE, TNF, HLA- DRB1 and HLA-DM (Adjusted p value <0.05). Also, the findings show that the genes involved in type 1 diabetes in the islets of Langerhans include CPE, MHC-II, and TNF-α.

    Conclusion

    The findings of this study showed that the increase in irradiation time in breast cancer cells probably leads to the activation of pathways related to type 1 diabetes through CPE, MHC-II and TNF-α genes in the islets of Langerhans.

    Keywords: Breast Cancer, Gene Ontology, Microarray, Irradiation, Type 1 Diabetes Mellitus
  • Alireza Panahi, Gholamreza Dadashi Oranj
    Introduction

     Agaricus blazei mushroom is used as a food and medicine, its effective composition is beta-glucan, which is used to treat some cancers and infections, including hepatitis C.Hepatitis C is an inflammatory disease that causes liver necrosis. Caspase2 protein is one of the factors promoting cell apoptosis and plays a role in tumor suppression. The purpose of this study is to determine the expression changes of the caspase2 gene and its effects on liver cancer.

    Materials and Methods

     In this project, raw expression data was obtained from the NCBI (National Center for Biotechnology Information) GEO (Gene Expression Omnibus) database section and using bioinformatics tools and methods and system biology such as Matlab (An abbreviation of "MATrix LABoratory), GEOR2 (Online software) and Cytoscape, the effect of consuming the desired mushroom on caspase2 gene expression was investigated.

    Results

     It was found that the beta-glucan combination has an increasing effect on target gene expression (p-value=0.05692).

    Conclusion

     The results show that the beta-glucan present in the mushroom can play a role as a prevention and even treatment of liver cancer by increasing the expression of caspase 2 protein by directing the damaged cell towards apoptosis.

    Keywords: Beta-glucan, Agaricus blazei, Hepatitis C, Caspase 2, Microarray, System biology
  • Hanieh Validad, Parvin Parvaie, Samira Nomiri, Ebrahim Miriâ€Moghaddam, Hossein Safarpour

    Primary Sjogren syndrome (PSS) is one of the most common systemic autoimmune diseases. Lymphocytic infiltration of exocrine glands, especially lacrimal and salivary in PSS, causes ocular and oral dryness. Dry mouth may lead to difficulty in speaking, chewing, and swallowing and result in reduced quality. The pathogenesis of PSS involves multiple factors, such as genetic, environmental, and immunological factors. Despite extensive research over the last few decades, the exact etiology and progression of PSS and its inflammatory lesions is still unknown. Gene co-expression network analysis (WGCNA) is a system biology method that can be used to describe the correlation between different genes and find modules of highly correlated genes and key genes. Also, by using these modules, we can get gene ontology information and biological pathways. In this study, we used WGCNA to analyze the GSE40611 dataset, which consists of 17 PSS patients and 18 healthy controls. We construct a co-expression network for mRNA expression data of patients and control groups and then find the most significant module and hub genes that play important roles in PSS. We also identify biological pathways and related miRNA for hub genes. Among all the modules, turquoise had the most correlation with PSS and some of the hub genes, including GPR18, FCRL1, VNN2 and etc. Also, a large number of pathways were identified in the turquoise module, most of them related to immune system activity, like T-cell activation, lymphocyte differentiation, leukocyte and lymphocyte activation, regulation of immune system processes, regulation of immune response, and cell-cell adhesion. External validation using bulk RNA sequencing data also confirmed the presence of selected hub-genes in pathogenicity of PSS. Finally, these results can lead to finding key players in treatment of PSS.

    Keywords: Primary Sjogren syndrome, Systems biology, WGCNA, Microarray, Bulk RNA sequencing
  • شیرین جلیلی*، محمد پنجی
    مقدمه
    اختلال افسردگی ماژور یکی از متداول ترین بیماری های حوزه روانی  است. نتایج پژوهش ها نشان می دهند که در این دسته از بیماران، فرآیندهای التهابی افزایش می یابند. با این وجود، شمار اندکی از پژوهش ها به موضوع مارکرهای التهابی در مغز این بیماران  پرداخته اند. هدف مطالعه حاضر بررسی بیان محور تنظیمی مرتبط با سیگنالینگ سیتوکین در بافت مغز بیماران مبتلا به اختلال افسردگی ماژور بود.
    روش کار
    با بهره گیری از یک رویکرد بیوانفورماتیکی بر پایه تجزیه و تحلیل داده های ریزآرایه، بیان یک محور تنظیمی در نمونه های بافت قشر پیش پیشانی بررسی شد. اصلاح پس زمینه، فیلتر کردن ژن و نرمال سازی داده ها با استفاده از آزمون های مختلف در نرم افزار R انجام شد. کیفیت داده ها نیز با بهره گیری از بسته AgiMicroRna و نمودار PCA بررسی شد. ژن های دارای تغییر بیان با استفاده از بسته limma  شناسایی شدند. برای بررسی همبستگی بین ژن های منتخب از آزمون پیرسون در نرم افزار R  استفاده شد.
    یافته ها
    نتایج بدست آمده نشان دادند که بیان ژن های BDNF و NRG1 در بافت PFC بیماران MDD با کاهش معناداری همراه بوده و از سوی دیگر بیان در سطح ژن های IL6 و TNF با افزایش معناداری روبرو شده است. همچنین یک همبستگی منفی قدرتمند میان ژن های IL6 و BDNF حاصل گردید.
    نتیجه گیری
    در این مطالعه، نتایج نشان می دهند که میان پیشرفت بیماری MDD و سیگنالینگ بواسطه سیتوکین رابطه پیچیده ای وجود دارد. این پژوهش شواهدی در راستای درک بهتر سازوکارهای بیماری زایی MDD ارایه می دهد.
    کلید واژگان: اختلال ماژور، بیوانفورماتیک، ریزآرایه، سیتوکین، قشر پیش پیشانی
    Shirin Jalili *, Mohammad Panji
    Introduction
    Major depressive disorder (MDD) is one of the most common mental illnesses. The results obtainedfrom previous studies conducted in this field show that inflammatory processes increase in MDD patients. However, few studies have addressed the issue of inflammatory markers in the brains of MDD patients. The aim of this study was to investigate the expression of regulatory axis related to cytokine signaling including IL6, TNF, NRG1 and BDNF in prefrontal cortex tissue samples.
    Materials and Methods
    In the present study, using a bioinformatics approach based on microarray data analysis, the expression of a regulatory axis related to cytokine signaling, including four genes (IL6, TNF, NRG1, and BDNF),in prefrontal cortex tissue (PFC) samples was investigated. Background correction, gene filtering and data normalization were done using different packages in R. Data quality was also evaluated using AgiMicroRna package and PCA plot.The limma package in R was used in order to identify the genes with expression changes. In addition, Pearson's correlation analysis was performed in R to check the correlation between the selected genes.
    Results
    The obtained results showed that the expression of BDNF and NRG1 genes in the PFC tissue of MDD patients was associated with a significant decrease (P= 0.037), and on the other hand, the expression of IL6 and TNF genes was significantly increased (P< 0.001). Also, a strong negative correlation between the IL6 and BDNF (P < 0.001) genes was obtained.
    Conclusion
    In this study, the results show that there is a complex relationship between MDD disease progressionand cytokine signaling. This research provides evidence for a better understanding of the mechanisms of MDD pathogenesis.
    Keywords: Major Disorder, Bioinformatics, Microarray, Cytokine, Prefrontal cortex
  • Nidhi Singh, Rinku Sharma, Sujoy Bose
    Aim

    This study aimed to identify key genes, non-coding RNAs, and their possible regulatory interactions during gallbladder cancer (GBC).

    Background

    The early detection of GBC, i.e. before metastasis, is restricted by our limited knowledge of molecular markers and mechanism(s) involved during carcinogenesis. Therefore, identifying important disease-associated transcriptome-level alterations can be of clinical importance.

    Methods

    In this study, six NCBI-GEO microarray dataseries of GBC and control tissue samples were analyzed to identify differentially expressed genes (DEGs) and non-coding RNAs {microRNAs (DEmiRNAs) and long non-coding RNAs (DElncRNAs)} with a computational meta-analysis approach. A series of bioinformatic methods were applied to enrich functional pathways, create protein-proteininteraction networks, identify hub genes, and screen potential targets of DEmiRNAs and DElncRNAs. Expression and interaction data were consolidated to reveal putative DElncRNAs:DEmiRNAs:DEGs interactions.

    Results

    In total, 351 DEGs (185 downregulated, 166 upregulated), 787 DEmiRNAs (299 downregulated, 488 upregulated), and 7436 DElncRNAs (3127 downregulated, 4309 upregulated) were identified. Eight genes (FGF, CDK1, RPN2, SEC61A1, SOX2, CALR, NGFR, and NCAM) were identified as hub genes. Genes associated with ubiquitin ligase activity, N-linked glycosylation, and blood coagulation were upregulated, while those for cell-cell adhesion, cell differentiation, and surface receptor-linked signaling were downregulated. DEGs-DEmiRNAs-DElncRNAs interaction network identified 46 DElncRNAs to be associated with 28 DEmiRNAs, consecutively regulating 27 DEGs. DEmiRNAs-hsa-miR-26b-5p and hsa-miR-335-5p; and DElnRNAs-LINC00657 and CTB-89H12.4 regulated the highest number of DEGs and DEmiRNAs, respectively.

    Conclusion

    The current study has identified meaningful transcriptome-level changes and gene-miRNA-lncRNA interactions during GBC and laid a platform for future studies on novel prognostic and diagnostic markers in GBC.

    Keywords: Gallbladder cancer, Microarray, Transcriptome, Differentially expressed genes, Differentially expressed microRNAs, Differentially expressed long non-coding RNAs
  • Haiyin Fan, Jin Zhang, Bin Zou, Zhisheng He*
    Background

    With the continuous advancement of diagnostic methods, more and more early-stage Non-small cell lung cancer (NSCLC) patients are diagnosed. Although many scholars have devoted substantial efforts to investigate the pathogenesis and prognosis of NSCLC, its molecular mechanism is still not well explained.

    Methods

    We retrieved three gene datasets GSE10072, GSE19188 and GSE40791 from the Gene Expression Omnibus (GEO) database and screened and identified differentially expressed genes (DEGs). Then, we performed KEGG and GO functional enrichment analysis, survival analysis, risk analysis and prognosis analysis on the selected hub genes. We constructed a protein-protein interaction (PPI) network, and used the STRING database and Cytoscape software.

    Results

    The biological process analysis showed that these genes were mainly enriched in cell division and nuclear division. Survival analysis showed that the genes of CEP55 (centrosomal protein 55), NMU (neuromedin U), CAV1 (Caveolin 1), TBX3 (T-box transcription factor 3), FBLN1 (fibulin 1) and SYNM (synemin) may be involved in the development, invasion or metastasis of NSCLC (P<0.05, logFC>1). Prognostic analysis and independent prognostic analysis showed that the expression of these hub gene-related mRNAs was related to the prognostic risk of NSCLC. Risk analysis showed that the selected hub genes were closely related to the overall survival time of patients with NSCLC.

    Conclusion

    The DEGs and hub genes screened and identified in this study will help us to understand the molecular mechanisms of NSCLC, and CEP55 expression affects the survival and prognosis of patients with NSCLC, and participates in tumor immune response.

    Keywords: CEP55, Microarray, NSCLC, Prognostic Model, Tumor Immune Response
  • میرزاعلی مفضل جهرمی، کیمیا رسولی پور، زهرا استخر، حامد میر، اباذر روستازاده*
    مقدمه

    انفارکتوس حاد میوکارد یکی از علل شایع مرگ و میر در دنیا است. هدف از مطالعه حاضر پیش بینی ارتباط ژن های اینترلوکین 17 و فاگوزوم با انفارکتوس حاد میوکارد بود.

    روش کار

    داده های ریزآرایه استخراج شده از مرکز ملی اطلاعات زیست فناوری (NCBI) توسط  نرم افزارهای GEO2R  و R  مورد تحلیل قرار گرفتند. ژن هایی که افزایش و کاهش بیان داشتند استخراج و با استفاده از پایگا های داده DAVID و Enrichr تحلیل عملکرد در مورد آن ها انجام شد.

    یافته ها

    در این مطالعه 208 ژن با Log2FC<-1 در گروه بیماران مبتلا به انفارکتوس حاد میوکارد در قیاس با گروه کنترل کاهش بیان داشتند. در این گروه ژن های PAQR8، CCR2،CCR5 و ZNF137P  به صورت معنادار بیان کمتری نسبت به بقیه ژن ها داشتند. همچنین 528 ژن با Log2FC>1 در قیاس با گروه کنترل به صورت معنادار افزایش بیان نشان دادند که در این گروه ژن های NR4A2، GABARAPL1، THBD، NFIL3 و MAFB نسبت به بقیه ژن ها بیان بالاتری داشتند. تحلیل KEGG بر روی ژن های دارای افزایش بیان نشان داد که مسیر پیام رسانی اینترلوکین 17و فاگوزوم در بروز بیماری انفارکتوس حاد میوکارد نقش دارد. 

    نتیجه گیری

    یافته های این مطالعه نشان داد، پس از بروز انفارکتوس حاد میوکارد، مسیرهای التهابی نظیر مسیر پیام رسانی اینترلوکین 17 احتمالا با بکار گیری پروتیین هایی همانند ماتریکس متالوپروتییناز 9 در ترمیم آسیب های بعد از انفارکتوس حاد میوکارد نقش دارد. همچنین فعال شدن فاگوزوم ها با واسطه مسیرهایی نظیر مولکول های سازگاری نسجی کلاس دو (MHC-II) و CD36 احتمالا در تسریع ترمیم آسیب های بعد از انفارکتوس حاد میوکارد نقش دارد.

    کلید واژگان: انفارکتوس حاد میوکارد، اینترلوکین 17، فاگوزوم، ریزآرایه
    Mirzaali Mofazzal Jahromi, Kimia Rasoolipoor, Zahra Estakhr, Hamed Mir, Abazar Roustazadeh*
    Introduction

    Acute myocardial infarction is one of the main causes of mortality in the worldwide. The aim of the present study is to predict the Association of interleukin (IL)-17 and phagosome with acute myocardial infarction.

    Methods and Materials:

    Microarray data were extracted from National Center for Biotechnology Information (NCBI) and then analyzed by GEO2R and R softwares. The functional analysis of up/down regulation of genes were performed using DAVID and Enrichr data bases.

    Results

    In this study, expression of 208 genes were lower in patients group compared to the controls (Log2FC<-1). In patients’ group, PAQR8, CCR2, CCR5, and ZNF137P genes significantly had lower expression. Although 528 gens, especially NR4A2, GABARAPL1, THBD, NFIL3, and MAFB significantly had more expression compared to the controls (Log2FC>+1). KEGG analysis on gens that increase expression showed that signaling pathways of IL-17 and phagosome are two pathways in patients with acute myocardial infarction.

    Conclusion

    According to our finding, after acute myocardial infarction, inflammatory pathway like IL-17 signaling recruiting matrix metalloproteinase 9 as a protein involve in repairing acute myocardial infarction damages. Also, the phagosome activity by major histocompatibility complex class-II (MHC-II) and CD36 signaling pathways, may be played a role in accelerating healing after acute myocardial infarction damages.

    Keywords: Acute Mocardial Infarction, IL-17, Phagosome, Microarray
  • B. Fatemeh Nobakht M. Gh, Yazdan Hasani Nourian, Masoud Arabfard *
    Background

    Nonalcoholic fatty liver disease (NAFLD) is the most common type of chronic liver disease worldwide. Left untreated, it can be a risk factor for developing cirrhosis or hepatocellular carcinoma (HCC). Although experts have made many efforts to find the underlying mechanisms of NAFLD, they remain a mystery.

    Objectives

    This study aimed to distinguish common gene signatures and pathways in the human liver during NAFLD progression through systems biology.

    Methods

    In this study, the researchers selected three microarray datasets, GSE48452, GSE63067, and GSE89632, from the NCBI GEO database to explore differentially expressed genes (DEGs) among healthy controls, simple steatosis, and nonalcoholic steatohepatitis (NASH) patients. Furthermore, protein-protein interaction (PPI) networks and pathway enrichment analyses were used to detect common genes and biological pathways in different stages of NAFLD.

    Results

    The current study included 45 healthy participants, 36 simple steatosis patients, and 46 NASH patients. Common genes for NAFLD progression were Chi3L1, ICAM1, MT1A, MT1H, ABCB11, ACOT1, CYP2C9, HSP90B1, and CPB2, which are involved in inflammation and oxidative stress pathways.

    Conclusions

    The present study investigated the shared vital genes and pathways between different stages of NAFLD, which may facilitate understanding NAFLD mechanisms and identifying potential therapeutic targets in this disease.

    Keywords: Systems Biology, Protein-protein Interaction Network, NAFLD, NASH, Microarray
  • Mohammad Hossein Derakhshan Nazari, Rana Askari Dastjerdi, Parnian Ghaedi Talkhouncheh, Ahmad Bereimipour, Hamidreza Mollasalehi, AmirAli Mahshad, Ali Razi, MohammadHossein Nazari, Amin Ebrahimi Sadrabadi *, Sara Taleahmad
    Objective

    Non-small cell lung adenocarcinoma (NSCLC) is the most common type of lung cancer, which is considered as the most lethal and prevalent cancer worldwide. Recently, molecular changes have been implicated to play a significant role in the cancer progression. Despite of numerous studies, the molecular mechanism of NSCLC pathogenesis in each sub-stage remains unclear. Studying these molecular alterations gives us a chance to design successful therapeutic plans which is aimed in this research.

    Materials and Methods

    In this bioinformatics study, we compared the expression profile of 7 minor stages of NSCLCadenocarcinoma, including GSE41271, GSE42127, and GSE75037, to clarify the relation of molecular alterations and tumorigenesis. At first, 99 common differentially expressed genes (DEG) were obtained. Then, functional enrichment analysis and protein-protein interaction (PPI) network construction were performed to uncover the association of significant cellular and molecular changes. Finally, gene expression profile interactive analysis (GEPIA) was employed to validate the results by RNA-seq expression data.

    Results

    Primary analysis showed that BMP4 was downregulated through the tumor progression to the stage IB andGPX2 was upregulated in the course of final tumor development to the stage IV and distant metastasis. Functional enrichment analysis indicated that BMP4 in the TGF-β signaling pathway and GPX2 in the glutathione metabolism pathway may be the key genes for NSCLC adenocarcinoma progression. GEPIA analysis revealed a correlation between BMP4 downregulation and GPX2 upregulation and lung adenocarcinoma (LUAD) progression and lower survival chances in LUAD patients which confirm microarray data.

    Conclusion

    Taken together, we suggested GPX2 as an oncogene by inhibiting apoptosis, promoting EMT and increasing glucose uptake in the final stages and BMP4 as a tumor suppressor via inducing apoptosis and arresting cell cycle in the early stages through lung adenocarcinoma (ADC) development to make them candidate genes to further cancer therapy investigations.

    Keywords: glutathione peroxidase, In silico, Microarray, NSCLC, TGF-β Signaling
  • غلامرضا داداشی اورنج، علیرضا پناهی*، جعفر رازقی
    پیش زمینه و هدف

    سرطان یک بیماری ژنتیکی است که به دنبال جهش در ژن های کنترل کننده ی فعالیت های سلول بروز می کند، سرطان پروستات یکی از شایع ترین انواع سرطان هایی است که در مردان دیده می شود. برای درمان این بیماری از جراحی، پرتودرمانی، هورمون درمانی و شیمی درمانی استفاده می گردد. این روش های درمانی عوارض متعدد بعد از درمان، ازجمله ناتوانی جنسی به همراه هزینه ی بالای درمان را به همراه دارند. لیکوپن یکی از آنتی اکسیدانت های موثر است که برای جلوگیری از رشد غده های سرطانی کاربرد دارد. پروتیین های BRCA1 و BRCA2 از مهارکننده های تومور هستند. این دو پروتیین با طیف وسیعی از فرآیندهای سلولی مانند ترمیم آسیب DNA، تنظیم رونویسی و بازسازی کروماتین مرتبط هستند. نقص در عملکرد BRCA1 و BRCA2 منجر به نقص در تعمیرات DNA می شود. این بی ثباتی در ژنوم، با انواع سرطان های سینه، تخمدان و پروستات در ارتباط است. در این تحقیق با استفاده از داده های میکروارری حاصل از بیوپسی بیماران مستعد به سرطان پروستات، تاثیر ترکیب لیکوپن بر روی بیان ژن های BRCA1 و BRCA2 موردبررسی قرار گرفته است.

    مواد و روش کار

    در این پروژه ی پژوهشی که به روش In Silico صورت گرفته، با استفاده از ابزارها و روش های بیوانفورماتیکی، تاثیر لیکوپن بر بیان ژن های BRCA1 و BRCA2 موثر در بروز سرطان پروستات مطالعه گردیده و تغییرات بیان این ژن های مهارگر موردسنجش قرار گرفته است. برای انجام این تحقیق داده های بیان ژن با حجم بالا از پایگاه NCBI بخش GEO دریافت شد، ازآنجاکه این داده های خام به کمک روش میکروارری استخراج و در پایگاه NCBI منتشر شده است، لذا متناسب باهدف این پژوهش، از داده های خام موجود استفاده گردید. برای آنالیز بهینه این داده ها با بهره گیری از نرم افزار Matlab، تغییرات بیان ژن های موردنظر تحت تیمار با ترکیب لیکوپن موردبررسی قرار گرفت. همچنین برای بررسی ارتباطات این ژن ها با همدیگر و دیگر ژن های موثر، از نرم افزار سیتو اسکپ استفاده گردیده است.

    یافته ها

    مطالعه بیوانفورماتیکی تاثیر لیکوپن بر ژن های BRCA1 و BRCA2 نشان داده است که این ترکیب بر بیان این پروتیین های مهارگر، اثر افزایشی داشته و در اثر تیمار بیماران با این ترکیب مقدار بیان این دو ژن افزایش پیدا کرده است.

    بحث و نتیجه گیری

     با توجه به آنالیز داده های میکروارری به صورت تثوریک، نتیجه گیری شد که ترکیب لیکوپن ازنظر تاثیر بر دو ژن مهارگر BRCA1 و BRCA2 به عنوان پیشگیری کننده و حتی درمان کننده سرطان پروستات می تواند مورداستفاده قرار گیرد.

    کلید واژگان: بیوانفورماتیک، بیان ژن، لیکوپن، سیتواسکپ، ارتباطات ژنی، سرطان، میکروارری
    Golamreza Dadashi Oranj, Alireza Panahi*, Jafar Razegi
    Background & Aims

    Cancer is a genetic disease that results from mutations in genes that control cell activities. Prostate cancer is one of the most common types of cancers in men. Surgery, radiation therapy, hormone therapy, and chemotherapy are used to treat this disease. These treatments have numerous side effects after treatment, including impotence along with the high cost of treatment. In this study, lycopene was studied as a carotenoid compound synthesized in plants. Lycopene is used by plants and microorganisms to Absorb of light is made during photosynthesis. Lycopene is one of the effective antioxidants used to prevent the growth of cancerous glands. BRCA1 and BRCA2 proteins are among tumor inhibitors. These two proteins are associated with various cellular processes such as DNA damage, repair, as well as with transcriptional regulation and chromatin regeneration. Defects in BRCA1 and BRCA2 function lead to defects in DNA repair. This instability in the genome is associated with a variety of breast, ovarian, and prostate cancers.

    Materials & Methods

    In this research project, In Silico method and bioinformatics tools were used to determine the effect of lycopene on the expression of BRCA1 and BRCA2 genes effective in prostate cancer, and the changes in the expression of these inhibitory genes have been measured. For this study, high volume gene expression data were obtained from the NCBI database, GEO section. As the raw data were extracted previously using microarray method and published in the NCBI database, so these raw data were used in accordance with the purpose of this study. For optimal analysis of these data, using Matlab software, the expression changes of the desired genes treated with lycopene were investigated. For determination of the communication of these genes with each other and with other effective genes, Cytoscape software has been used.

    Results

    Bioinformatics study of the effect of lycopene on BRCA1 and BRCA2 genes has shown that this combination has an increasing effect on the expression of these inhibitory proteins. therefore, treatment of patients with this combination, the expression of BRCA1 and BRCA2 genes has increased.

    Conclusion

    Based on theorical analysis of microarray data, it was concluded that lycopene can be used as a preventive and even a treatment for prostate cancer in terms of its effect on BRCA1 and BRCA2 inhibitor genes.

    Keywords: BRCA1, BRCA2, Insilico, Microarray, Lycopene, Prostate, Genetic Interaction, Cytoscape
  • Gholamreza Dadashi Oranj*
    Introduction

     Yellow fever virus causes systemic disease of the liver, kidneys, myocardium and hemorrhage, which are high incidence and mortality. Lycopene is one of the effective antioxidants used to prevent the growth of cancerous tumors. DNAJC14 protein is a variant of heat shock protein (chaperone) Hsp40. Hsp40 chaperone protein (DNAJC14) that when overexpressed was able to mediate protection from yellow fever virus (YFV)-induced cell death. In this study, to find a new treatment for yellow fever, the effect of lycopene on the expression of DNAJC14 gene involved in yellow fever was investigated.

    Materials and methods

    In this project, using bioinformatics software, such as Matlab and Cytoscape, the effect of lycopene on the expression of DNAJC14 gene, as well as the relationship of this gene with different genes have been investigated. Big gene expression data in the NCBI database were used for this study.

    Results

    Analysis of microarray data showed that the expression level of DNAJC14 gene was increased under the influence of lycopene.

    Conclusion

     The lycopene combination can be used as a preventative and even treatment for yellow fever viral disease due to the effect DNAJC14 gene expression.

    Keywords: Lycopene, Yellow fever, Bioinformatics, Co- expression, Microarray, Cytoscape
  • مهدی کریمی، اباذر روستازاده*
    مقدمه

    پره اکلامپسی یک بیماری هتروژنوس در دوره بارداری می باشد که پاتوفیزیولوژی دقیق آن مشخص نیست .امروزه اگزوزوم ها به عنوان یکی از عوامل دخیل در پاتوژنز این بیماری مطرح است.  هدف از مطالعه کنونی جستجو در کتابخانه های ریزآرایه و انجام آنالیز عملکرد بر روی ژن های استخراج شده بود تا نقش آنها در پاتوژنز پره اکلامپسی را پیش بینی نماییم.

    روش کار

    داده های ریز آرایه GSE10588 توسط GEO2R و نرم افزار R (نسخه 4.1.0) آنالیز شدند. تجزیه و تحلیل اجزای اصلی (PCA) برای بررسی نرمال بودن داده ها انجام گرفت. آنالیز عملکرد توسط Enrichr و DAVID 6.8  و    PANTHER 16 انجام گرفت.

    یافته ها

    آنالیز داده های ریز آرایه نشان داد که ژن های LEP ، OR8G2 و DST بیشترین میزان بیان و ژن های PTCH1 و ZNF598 کمترین بیان را در جفت زنان مبتلا به پره اکلامپسی دارند. آنالیز اجزای سلولی نشان داد که بیشترین تعداد ژن های استخراج شده مرتبط با اگزوزوم خارج سلولی می باشد. بعلاوه پاسخ به هیپوکسی ، اتصال سلول به سلول ، تکامل مغز و متابولیسم گالاکتوز مسیرهای استخراج شده می باشند.

    نتیجه گیری

    اگزوزوم خارج سلولی ، پاسخ به هیپوکسی و متابولیسم گالاکتوز نیاز به توجه و بررسی بیشتری در پره اکلامپسی دارند.

    کلید واژگان: آنالیز عملکرد، ریز آرایه، پره اکلامپسی، حاملگی
    Mahdi Karimi, Abazar Roustazadeh*
    Background

     Preeclampsia (PE) is a heterogeneous pregnancy disease which the exact pathophysiology of it is unknown. Recently exosomes have been indicated as a causative factor in the pathogenesis of PE. The aim of the study was to investigate in microarray library data to extract the differentially expressed genes (DEGs) in PE and to perform a functional enrichment analysis to predict the role of DEGs in pathogenesis of PE.

    Materials and methods

    GSE10588 microarray library data was analyzes by GEO2R and R package (version 4.1.0). Principal component analysis (PCA) was performed to analyze the normality of the data. Annotation analysis was performed by Enrichr, DAVID 6.8 and PANTHER 16.

    Results

    Microarray data analysis showed that LEP, OR8G2 and DST genes had the highest expression and PTCH1 and ZNF598 genes had the lowest expression in placenta of preeclamtic women. Cellular component analysis showed that most of the extracted genes are related to extracellular exosome. In addition, response to hypoxia, cell-cell adhesion, brain development and galactose metabolism are the pathways that enriched.

    Conclusion

    Extracellular exosome, response to hypoxia and galactose metabolism need more attention and investigation in PE.

    Keywords: Functional enrichment analysis, Microarray, Preeclampsia, Pregnancy
  • Arsalan Jalili, Abbas Hajifathali, Ahmad Bereimipour, Elham Roshandel, Nasser Aghdami
    Objective

    Different Cell Culture medias can affect the expansion of T cells. The aim of this study is to assess signaling pathways, protein interactions and genes in T cells cultured in different common T cell expansion medias to select the best candidate.

    Materials and Methods

    In this in silico observational study, with the use of bioinformatics analysis and the use of enrichment databases, gene expression profiles were investigated using microarray analysis.

    Results

    The results of this study were the joint selection of 26 upregulated genes and 59 downregulated genes that were involved in SREBP control of lipid synthesis, co-stimulatory signal during T-cell activation mitosis and chromosome dynamics, telomeres, telomerase, and cellular aging signal pathways.

    Conclusion

    Using bioinformatics analyzes, integrated and regular genes were selected as common genes CD80, LST1, ATM and ITM2B 4-1BBL, Akt inhibitor, interleukin 7 and 15 expansion media.

    Keywords: Expansion, Microarray, TCD8+Cells
  • Luis Miguel Paco Meza, Mdolores Carmona, Sagrario Canadillas, Ana Lopez Diaz, Francisco Munoz Lopez, Alvaro Jimenez Arranz, Ipek Guler, Concha Herrera *
    Objective(s)

    Adipose tissue-derived mesenchymal stromal cells (ASCs) are useful in cell-based therapy.  However, it is well known that diabetes mellitus (DM) alters ASCs’ functionality. The majority of in vitro studies related to ASCs are developed under non-physiological oxygen conditions. Therefore, they may not reflect the full effects of DM on ASCs, in vivo. The main aim of the current study is to identify molecular pathways and underlying biological mechanisms affected by diabetes on ASCs in physiological oxygen conditions.

    Materials and Methods

    ASCs derived from healthy (ASCs-C) and diabetic (ASCs-D) rats were expanded under standard culture conditions (21% O2) or cultured in physiological oxygen conditions (3% O2) and characterized. Differential gene expressions (DEGs) of ASCs-D with respect to ASCs-C were identified and analyzed with bioinformatic tools. Protein-protein interaction (PPI) networks, from up- and down-regulated DEGs, were also constructed.

    Results

    The bioinformatic analysis revealed 1354 up-regulated and 859 down-regulated DEGs in ASCs-D, with 21 and 78 terms over and under-represented, respectively. Terms linked with glycosylation and ribosomes were over-represented and terms related to the activity of RNA-polymerase II and transcription regulation were under-represented. PPI network disclosed RPL11-RPS5 and KDR-VEGFA as the main interactions from up- and down-regulated DEGs, respectively.

    Conclusion

    These results provide valuable information about gene pathways and underlying molecular mechanisms by which diabetes disturbs ASCs biology in physiological oxygen conditions. Furthermore, they reveal, molecular targets to improve the use of ASCs in autologous transplantation.

    Keywords: Cell-based therapy, Diabetes, Enrichment analysis, Microarray, Physioxia
  • محسن علی پور، اباذر روستازاده*
    مقدمه

    پاندمی کووید 19 عده کثیری را مبتلا نموده و متاسفانه موجب مرگ و میر بسیاری نیز شده است. مکانیسم دقیق عمل ویروس عامل آن در بدن مشخص نیست. هدف از مطالعه کنونی بررسی و آنالیز داده های ریز آرایه و بررسی عملکرد بود تا بتوانیم به مکانیسم های جدید نحوه عملکرد این ویروس در سلول های انسان دست یابیم.

    روش کار

    داده های ریزآرایه استخراج شده از NCBI توسط GEO2R و نرم افزار R مورد آنالیز قرار گرفت. ژن هایی که افزایش بیان و کاهش بیان داشتند استخراج شدند و سپس آنالیز عملکرد در مورد آنها صورت گرفت .

    یافته ها

    . نتایج نشان داد که در سطح لگاریتم پایه دو تغییر بیان بزرگتر از 3 و کوچکتر از 3- ترانس کریپتوم، 319 و 573 ژن افزایش بیان یافته به ترتیب در گروه بیماران کووید خفیف و کووید شدید وجود دارند. همچنین 156 و 590 ژن کاهش بیان یافته به ترتیب در گروه بیماران کووید خفیف و کووید شدید وجود دارند. نتایج GO نشان داد که الگوی ژن های تفاوت بیان یافته در گروه بیماران کووید با فرم شدید با ژن ATP13A2 مرتبط است.

    نتیجه گیری

    ویروس کووید 19 احتمالا در تعامل با عواملی چون ATP13A2 شرایط بقای خود در داخل سلول را تنظیم می نماید.

    کلید واژگان: کووید 19، ریز آرایه، ATP13A2، آنالیز عملکرد
    Mohsen Alipour, Abazar Roustazadeh *
    Introduction

    Unfortunately, a lot of people infected with and died due to covid-19. The exact mechanism of causative virus in human body is unknown. The aims of the study were to survey and analysis the microarray data and to perform functional analysis to unveil the new mechanisms of this virus in regarding to human cells.

    Methods

    NCBI microarray extracted data were analyzed by GEO2R and R package. Up- and down-regulated genes were extracted and functional analysis was performed.

    Results

    results showed that in Log of expression greater than 3 and lesser than -3 of transcriptome, there were 319 and 573 up-regulated genes in mild and severe covid-19 patients, respectively. Also there were 156 and 590 down-regulated genes in mild and severe covid-19 patients, respectively. GO analysis showed that deferentially expressed gene pattern in severe covid-19 patients is related to ATP13A2

    Conclusion

    Covid-19 probably regulates its vitality in human cells through interplay with factors such as ATP13A2

    Keywords: Covid-19, Microarray, ATP13A2, Functional analysis
  • Khyber Shinwari, Mikhail A. Bolkov, Irina A. Tuzankina, Valery A. Chereshnev

    HOIL-1/RBCK1 deficiency is a new autosomal receive disorder with unstable cellular responses to pro-inflammatory cytokines, resulting in auto-inflammation, pyogenic bacterial disease, as well as the development of muscular amylopectinosis. This study explored the molecular mechanisms of RBCK1 deficiency with integrated bioinformatics analyses of the feature genes and the correlative gene functions. The expression profile of GSE24519 was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) between RBCK1, MYDK88, NEMO deficient fibroblast, and healthy fibroblast specimens were identified. Gene ontology (GO) enrichment analysis on gene functions and the Kyoto Encyclopedia of Gene and Genome (KEGG) pathway analysis were performed by using Database for Annotation, Visualization, and Integrated Discovery (DAVID). Cytoscape was used to visualize the protein-protein interaction (PPI) of these DEGs. GO analysis revealed that the “Skeletal system development, Extracellular matrix organization, Positive regulation of cell migration, Negative regulation of canonical Wnt signaling pathway, Cell adhesion, Angiogenesis and Negative regulation of BMP signaling pathway, Serine-type carboxypeptidase activity, Polysaccharide binding, Calcium ion binding, frizzled binding, Neuropilin binding, and cell adhesion molecule binding, extracellular exosome, extracellular space, extracellular region, lysosomal lumen, endoplasmic reticulum lumen, cell surface and focal adhesion to BP, MF, and CC, respectively. The KEGG pathway analysis showed that the complement and coagulation cascade, ECM receptor interactions, PI3K- Akt signaling pathway, PPAR signaling pathway, TGF-beta signaling pathway, Pathway in Cancer, Viral carcinogenesis and Focal adhesion pathway were closely associated with RBCK1 deficiency occurrence. Importantly, TK1, AURKB, CDCA2, UBE2C, KIFC1, CEP55, CDCA3, GINS2, MCM6, and CDC45 were predicted to be significantly related to RCBK1 deficiency. Our discovery provides a registry of genes and pathways that are disrupted in RCBK1, which will enhance in understanding the pathogenesis of RBCK1 deficiency and other innate immunodeficiency diseases. This study has the potential to be used in the clinic for diagnosis and targeted therapy of RCBKI and other innate immunodeficiencies in the future.

    Keywords: Primary immunodeficiency, RBCK1 deficiency, Differential expressed genes, Key pathways, Hub genes, Microarray
  • Sepideh Kadkhoda, Farzaneh Darbeheshti, Nima Rezaei*, Ghasem Azizi-Tabesh, Faezeh Zolfaghari, Sadollah Tavakolibazaz, Reza Taslimi, Javad Tavakkoly-Bazzaz
    Aim

    The aim of this study was to integrate both coding and non-coding available microarray data in the development of colorectal cancer (CRC) with bioinformatics analyses to attain a more inclusive pathobiologic map of their molecular interactions and functions.

    Background

    Identification of competing endogenous RNAs (ceRNAs), especially circRNAs, has become a new hotspot in cancer research, although their roles and underlying mechanisms in CRC development remain mostly unknown.

    Methods

    Microarray data was retrieved from the Gene Expression Omnibus (GEO) database and analyzed. Several bioinformatics tools and databases were applied for further elucidation. Principal component analysis (PCA) was run separately for four datasets. The dysregulated circRNA-miRNA-mRNA, co-expression, and protein-protein interaction (PPI) networks were established.

    Results

    PCA discloses colorectal tumors; normal tissue can be distinguished not only by mRNAs expression profile, but also by both circRNA and miRNA expression profiles. In this study, 14 DE mRNAs, 85 DE miRNAs, and 36 DE circRNAs were identified in CRC tissue and compared with normal tissue. Taking their potential interactions into account, a circRNA-miRNA-mRNA network was constructed. The results disclosed some DE circRNAs with potential oncogenic (circ_0014879) or tumor suppressive (circ_0001666 and circ_0000977) effects. Finally, the PPI network suggests pivotal roles for DOCK2 and PTPRC dysregulation in the progression of CRC, possibly by facilitating tumor escape from immune surveillance.

    Conclusion

    The current study proposes a novel regulatory network consisting of DE circRNAs, miRNAs, and mRNAs in CRC development that highlights the roles of DE circRNAs at the upstream of oncotranscriptomic cascade in CRC development, suggesting their potential to be utilized as both prognostic and therapeutic biomarkers.

    Keywords: circRNA, miRNA, Colorectal cancer, Microarray, Bioinformatics
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