scholarly journals Autophagy-Related Long Non-coding RNA Signature as Indicators for the Prognosis of Uveal Melanoma

2021 ◽  
Vol 12 ◽  
Author(s):  
Yi Cui ◽  
Mi Zheng ◽  
Jing Chen ◽  
Nuo Xu
Keyword(s):  
High Risk ◽  
Signaling Pathway ◽  
Uveal Melanoma ◽  
Killer Cell ◽  
Differentially Expressed ◽  
Receptor Signaling ◽  
Regression Analyses ◽  
Non Coding Rna ◽  
Receptor Signaling Pathway ◽  
Long Non Coding Rna

This study aimed to develop an autophagy-associated long non-coding RNA (lncRNA) signature to predict the prognostic outcomes of uveal melanoma (UM). The data of UM from The Cancer Genome Atlas (TCGA) were enrolled to obtain differentially expressed genes (DEGs) between metastasizing and non-metastasizing UM patients. A total of 13 differentially expressed autophagy genes were identified and validated in Gene Expression Omnibus, and 11 autophagy-related lncRNAs were found to be associated with overall survival. Through performing least absolute shrinkage and selection operator regression analyses, a six-autophagy-related lncRNA signature was built, and its efficacy was confirmed by receiver-operating characteristic, Kaplan–Meier analysis, and univariate and multivariate Cox regression analyses. A comprehensive nomogram was established and its clinical net benefit was validated by decision curve analysis. GSEA revealed that several biological processes and signaling pathways including Toll-like receptor signaling pathway, natural killer cell-mediated cytotoxicity, and B- and T-cell receptor signaling pathway were enriched in the high-risk group. CIBERSORT results showed that the signature was related to the immune response especially HLA expression. This signature could be deployed to assist clinicians to identify high-risk UM patients and help scientists to explore the molecular mechanism of autophagy-related lncRNAs in UM pathogenesis.

LincRNA Expression Discriminates Cytogenetic Subtypes In B-Lymphoblastic Leukemia and Plays a Functional Role In Leukemia Cell Survival

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 2570-2570
Author(s):  
Waters Ella ◽  
Thilini R Fernando ◽  
Norma Iris Rodriguez-Malave ◽  
Weihong Yan ◽  
Martina Pigazzi ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Functional Role ◽  
Lymphoblastic Leukemia ◽  
Differentially Expressed ◽  
Receptor Signaling ◽  
Prednisolone Treatment ◽  
Non Coding Rna ◽  
Receptor Signaling Pathway

Abstract It has now become clear that a recently described class of non-coding RNA, so-called long intergenic non-coding RNA (lincRNA), has a vital role in gene regulation. Dysregulation of their expression has been shown to be associated with the development of cancers. However, the role of lincRNAs in B-lymphoblastic leukemia (B-Acute Lymphoblastic Leukemia; B-ALL) has not been investigated thus far. Here, we analyzed lincRNA expression in B-ALL samples to investigate their role in pathogenesis and disease severity. Using microarray technology, we analyzed 44 cases of B-ALL of three different cytogenetic subtypes, namely t(12;21), TEL-AML1 translocated; t(1;19) E2A-PBX translocated; and 11q23 (MLL)-rearranged cases and found that lincRNAs were expressed in distinctive patterns across the 3 different cytogenetic subtypes. We named the top 10 differentially expressed lincRNAs as B-ALL associated long intergenic RNAs, or BALIRs. Using RT-qPCR, differential lincRNA expression was confirmed in both the original samples and in an independent cohort. In both original and independent samples, four lincRNAs were consistently differentially expressed in cases with MLL rearrangement, which constitute a poor prognostic subgroup in B-ALL. We also found that the expression of BALIR-2 and BALIR-6, two of the four lincRNAs that we queried by RT-qPCR, was significantly different in prepreB immunophenotype. Looking at clinicopathologic correlates for the patients in these studies, we found that BALIR-2 was significantly higher in patients who had poor survival and diminished response to prednisone treatment. We further characterized BALIR-2 using B-ALL cell lines. The chromosomal location of BALIR-2 was conserved in mice and humans. Using RACE, we confirmed the 5’ and the 3’ end of the transcript. In order to further characterize the prednisone response in the patients, we treated RS411and NALM6 cell lines with prednisolone. We found a 30-50% decrease in expression of BALIR-2 following prednisolone treatment. Next, we knocked down BALIR-2 expression using a lentiviral miRNA-formatted siRNA system. BALIR-2 knockdown resulted in reduced cell proliferation and a modest increase in apoptosis of B-ALL cell lines both at steady state and when treated with prednisolone. To examine the mechanism by which BALIR-2 affects proliferation and apoptosis in B-ALL cell lines, we examined gene expression by microarray in RS411 cell lines with BALIR-2 knockdown with and without prednisolone treatment. Clustering analyses revealed several differentially expressed genes; of these, one of the top clusters included genes involved in the prednisolone response / glucocorticoid receptor signaling pathway (HSPA6, SGK1, IL8, JUN, SERPINE1, CDKN1A and ICAM1). We are currently confirming the expression of several of these genes in multiple cell lines by RT-qPCR and Western Blotting. In conclusion, this data suggests that BALIR-2 may play a functional role in the survival of B-ALL cells and thereby contribute to the inferior survival observed in patients with high levels of BALIR-2 expression. Based on the microarray experiments, BALIR-2 may be regulating the expression of glucocorticoid receptor signaling pathway genes and thereby apoptosis. These results suggest that knockdown of BALIR-2 could be utilized as a therapeutic approach in treating B-ALL, particularly in poor-prognostic group cases with MLL rearrangement. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Analyses of long non-coding RNA and mRNA profiling in the spleen of diarrheic piglets caused by Clostridium perfringens type C

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5997 ◽  
Author(s):  
Zunqiang Yan ◽  
Xiaoyu Huang ◽  
Wenyang Sun ◽  
Qiaoli Yang ◽  
Hairen Shi ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Clostridium Perfringens ◽  
Diarrheal Disease ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Mapk Signaling ◽  
Non Coding Rna ◽  
Receptor Signaling Pathway ◽  
Type C ◽  
Long Non Coding Rna

Background Clostridium perfringens (C. perfringens) type C is the most common bacteria causing piglet diarrheal disease and it greatly affects the economy of the global pig industry. The spleen is an important immune organ in mammals; it plays an irreplaceable role in resisting and eradicating pathogenic microorganisms. Based on different immune capacity in piglets, individuals display the resistance and susceptibility to diarrhea caused by C. perfringens type C. Recently, long non-coding RNA (lncRNA) and mRNA have been found to be involved in host immune and inflammatory responses to pathogenic infections. However, little is known about spleen transcriptome information in piglet diarrhea caused by C. perfringens type C. Methods Hence, we infected 7-day-old piglets with C. perfringens type C to lead to diarrhea. Then, we investigated lncRNA and mRNA expression profiles in spleens of piglets, including control (SC), susceptible (SS), and resistant (SR) groups. Results As a result, 2,056 novel lncRNAs and 2,417 differentially expressed genes were found. These lncRNAs shared the same characteristics of fewer exons and shorter length. Bioinformatics analysis identified that two lncRNAs (ALDBSSCT0000006918 and ALDBSSCT0000007366) may be involved in five immune/inflammation-related pathways (such as Toll-like receptor signaling pathway, MAPK signaling pathway, and Jak-STAT signaling pathway), which were associated with resistance and susceptibility to C. perfringens type C infection. This study contributes to the understanding of potential mechanisms involved in the immune response of piglets infected with C. perfringens type C.

scholarly journals Aberrant expression of long non-coding RNA in thyroid neoplasms

2019 ◽  
pp. 17-25
Author(s):  
В.Д. Якушина ◽  
А.С. Танас ◽  
А.В. Лавров
Keyword(s):  
Thyroid Cancer ◽  
Signaling Pathway ◽  
In Silico ◽  
Thyroid Nodules ◽  
Differentially Expressed ◽  
Follicular Variant ◽  
Aberrant Expression ◽  
Lncrna Expression ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Актуальность. Длинные некодирующие РНК (днРНК) при раке щитовидной железы плохо изучены; не известны днРНК, общие и специфичные для фолликулярного и классического вариантов папиллярного рака, не установлены днРНК, аберрантно экспрессированные при других основных субтипах злокачественных новообразований щитовидной железы, а также при доброкачественных новообразованиях. Цель исследования - определить днРНК, аберрантно экспрессированные при фолликулярной аденоме (ФА), фолликулярном раке (ФРЩЖ), фолликулярном и классическом вариантах папиллярного рака (ПРЩЖ), анапластическом раке (АРЩЖ) щитовидной железы. Методы. Проанализирована экспрессия днРНК по данным исследований на микрочипах (8 независимых экспериментов, доступных в GEO) и секвенирования РНК (PRJEB11591 и TCGA-THCA). Исследованы 246 образцов нормальной ткани щитовидной железы, 26 - ФА, 30 - ФРЩЖ, 181 - фолликулярного варианта ПРЩЖ, 481 - классического варианта ПРЩЖ и 49 - АРЩЖ. Для классического и фолликулярного вариантов ПРЩЖ выполнена валидация дифференциальной экспрессии in silico. Потенциальные биологические функции были оценены в результате анализа обогащения коэкспрессированных генов. Результаты. Определены днРНК, дифференциально экспрессированные при ФА, ФРЩЖ, фолликулярном и классическом вариантах ПРЩЖ и АРЩЖ. Выявлены 8 днРНК, экспрессия которых изменена во всех субтипах новообразований щитовидной железы, 22 - общих для ПРЩЖ, 32 - специфичных для классического варианта ПРЩЖ, 1 - специфичная для фолликулярного варианта ПРЩЖ, и 177 - специфичных для АРЩЖ. Статистически значимо дифференциально экспрессированных днРНК в ФРЩ по сравнению с ФА не выявлено. Ранее известные онкогенные и супрессорные днРНК NR2F1-AS1, LINC00511, SLC26A4-AS1, CRNDE, RMST впервые обнаружены в новообразованиях щитовидной железы. Выявленные днРНК предположительно вовлечены в клеточную адгезию, организацию экстрацеллюлярного матрикса, образование эндодермы, регуляцию клеточного цикла и митоза, полярности клеток, сигнальные пути VEGF и WNT. Выводы. Установлены общие и специфичные паттерны экспрессии днРНК в доброкачественных и злокачественных новообразованиях щитовидной железы. Background. Long non-coding RNA (lncRNA) in thyroid cancer are poorly investigated; no lncRNAs common and specific for the follicular and classical variants of papillary cancer, as well as no lncRNAs aberrantly expressed in benign nodules or other subtypes of thyroid cancer are established. The objective of the study is to determine long noncoding RNAs aberrantly expressed in follicular adenoma (FA), follicular carcinoma (FTC), follicular and classical variants of papillary carcinoma (PTC), anaplastic carcinoma (ATC). Methods. lncRNA expression was analyzed in dataset of Microarray (8 independent experiments available in GEO) and RNA-seq studies (PRJEB11591 and TCGA-THCA). In total, 246 samples of normal thyroid tissue, 26 FAs, 30 FTCs, 181 follicular variant PTCs, 481 classic variant PTCs and 49 ATCs were examined. In silico validation was performed. Potential biological functions were assessed by enrichment analysis of coexpressed genes. Results. LncRNAs differentially expressed in FA, FTC, follicular, and classical variants of PTC, and ATC are identified. There are 8 lncRNAs common for all investigated thyroid nodules, 22 common for PTC, 32 specific for classical PTC, 1 specific for follicular variant of PTC, and 177 specific for ATC. No lncRNA significantly differentially expressed in FTC compared to FA is identified. The previously described oncogenic and suppressor lncRNAs NR2F1-AS1, LINC00511, SLC26A4-AS1, CRNDE, RMST are detected in thyroid carcinomas for the first time. Identified lncRNA are putatively involved in cell adhesion, extracellular matrix organization, endoderm formation, VEGF signaling pathway, WNT signaling pathway and cell polarity, cell cycle and mitosis. Conclusion. The general and specific patterns of lncRNA expression in benign and malignant thyroid nodules are established.

scholarly journals Host Non-Coding RNA Regulates Influenza A Virus Replication

Viruses ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 51
Author(s):  
Yuejiao Liao ◽  
Shouqing Guo ◽  
Geng Liu ◽  
Zhenyu Qiu ◽  
Jiamin Wang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Influenza A Virus ◽  
Influenza A ◽  
Janus Kinase ◽  
Research Progress ◽  
Receptor Signaling ◽  
Non Coding Rna ◽  
Receptor Signaling Pathway ◽  
Non Coding Rnas ◽  
Virus Interactions

Outbreaks of influenza, caused by the influenza A virus (IAV), occur almost every year in various regions worldwide, seriously endangering human health. Studies have shown that host non-coding RNA is an important regulator of host–virus interactions in the process of IAV infection. In this paper, we comprehensively analyzed the research progress on host non-coding RNAs with regard to the regulation of IAV replication. According to the regulation mode of host non-coding RNAs, the signal pathways involved, and the specific target genes, we found that a large number of host non-coding RNAs directly targeted the PB1 and PB2 proteins of IAV. Nonstructural protein 1 and other key genes regulate the replication of IAV and indirectly participate in the regulation of the retinoic acid-induced gene I-like receptor signaling pathway, toll-like receptor signaling pathway, Janus kinase signal transducer and activator of transcription signaling pathway, and other major intracellular viral response signaling pathways to regulate the replication of IAV. Based on the above findings, we mapped the regulatory network of host non-coding RNAs in the innate immune response to the influenza virus. These findings will provide a more comprehensive understanding of the function and mechanism of host non-coding RNAs in the cellular anti-virus response as well as clues to the mechanism of cell–virus interactions and the discovery of antiviral drug targets.

scholarly journals Long Noncoding RNA Expression Profile in BV2 Microglial Cells Exposed to Lipopolysaccharide

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Yajuan Li ◽  
Qingmin Li ◽  
Cunjuan Wang ◽  
Shengde Li ◽  
Lingzhi Yu
Keyword(s):  
Neuropathic Pain ◽  
Signaling Pathway ◽  
Noncoding Rna ◽  
Cell Activation ◽  
Differentially Expressed ◽  
Microglial Cells ◽  
Receptor Signaling ◽  
Microglia Cell ◽  
Receptor Signaling Pathway

Neuropathic pain, which is one of the most common forms of chronic pain, seriously increases healthcare costs and impairs patients’ quality of life with an incidence of 7–10% worldwide. Microglia cell activation plays a key role in the progression of neuropathic pain. Better understanding of novel molecules modulating microglia cell activation and these underlying functions will extremely benefit the exploration of new treatment. Recent studies suggested long noncoding RNAs may be involved in neuropathic pain. However, its underlying functions and mechanisms in microglia cell activation remain unclear. To identify the differentially expressed lncRNAs and predict their functions in the progression of microglia cell activation, GSE103156 was analyzed using integrated bioinformatics methods. The expression levels of selected lncRNAs and mRNAs were determined by real-time PCR. In the present study, a total of 56 lncRNAs and 298 mRNAs were significantly differentially expressed. The differentially expressed mRNAs were mainly enriched in NF-kappa B signaling pathway, TNF signaling pathway, Toll-like receptor signaling pathway, and NOD-like receptor signaling pathway. The top 10 hub genes were Tnf, Il6, Stat1, Cxcl10, Il1b, Tlr2, Irf1, Ccl2, Irf7, and Ccl5 in the PPI network. Our results showed that Gm8989, Gm8979, and AV051173 may be involved in the progression of microglia cell activation. Taken together, our findings suggest that lots of lncRNAs may be involved in BV2 microglia cell activation in vitro. The findings may provide relevant information for the development of promising targets for the microglial cells activation of neuropathic pain in vivo in the future.

Identification of DMSA-Coated Fe3O4 Nanoparticles Induced-Apoptosis Response Genes in Human Monocytes by cDNA Microarrays

2013 ◽  
Vol 749 ◽  
pp. 377-383 ◽  
Author(s):  
Ying Xun Liu ◽  
Jian Yuan Huang ◽  
Dong Liang Wang ◽  
Jin Ke Wang
Keyword(s):  
Gene Expression ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Differentially Expressed ◽  
Dependent Manner ◽  
Receptor Signaling ◽  
Apoptosis Pathway ◽  
Receptor Signaling Pathway

This study investigated the cell apoptosis and gene expression profiles of human THP-1 monocytes in order to identify the molecular mechanism of cell apoptosis induced by meso-2,-3-dimercaptosuccinnic acid-coated Fe3O4magnetic nanoparticles. Cell apoptosis was visualized with flow cytometry after treated by 50 and 100 μg/ml Fe3O4nanoparticles, and the gene expression profiles were detected with Affymetrix Human Genome U133 Plus 2.0 GeneChips® microarrays. The transmission electron microscopy obserbation revealed that THP-1 cells were effectively labeled by the Fe3O4nanoparticles. The internalized Fe3O4nanoparticles increased cell apoptosis in a dose-dependent manner, but not decreased cell viability significantly. The cDNA microarray results showed that hundreds of genes were significantly regulated at the concentration of 50 and 100 μg/ml, and the level of these genes exhibited a dose response, includingCD14,CD86,CFLAR,IL-1,NFKBIA,NLRC4,NAIPandAIP3. The Fe3O4nanoparticles treatments resulted in significantly altered in Toll-like receptor signaling pathway, NOD-like receptor signaling pathway, and Cell apoptosis signaling pathway. Gene ontology analysis of these differentially expressed genes demonstrated that mainly up-regulated genes were related to cytokine production and cell apoptosis. These results showed that the Fe3O4nanoparticles induced THP-1 cells apoptosis and the level of lots of genes involved in extrinsic apoptosis pathway differentially expressed, which further revealed demonstrated the relation between Fe3O4MNPs treatment and cell apoptosis.

scholarly journals Identification of potential microRNAs and KEGG pathways in denervation muscle atrophy based on meta-analysis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xinyi Gu ◽  
Bo Jin ◽  
Zhidan Qi ◽  
Xiaofeng Yin
Keyword(s):  
Signaling Pathway ◽  
Muscle Atrophy ◽  
Meta Analysis ◽  
Cell Receptor ◽  
Differentially Expressed ◽  
Receptor Signaling ◽  
Denervated Muscle ◽  
Kegg Pathways ◽  
Receptor Signaling Pathway ◽  
Cell Receptor Signaling

AbstractThe molecular mechanism of muscle atrophy has been studied a lot, but there is no comprehensive analysis focusing on the denervated muscle atrophy. The gene network that controls the development of denervated muscle atrophy needs further elucidation. We examined differentially expressed genes (DEGs) from five denervated muscle atrophy microarray datasets and predicted microRNAs that target these DEGs. We also included the differentially expressed microRNAs datasets of denervated muscle atrophy in previous studies as background information to identify potential key microRNAs. Finally, we compared denervated muscle atrophy with disuse muscle atrophy caused by other reasons, and obtained the Den-genes which only differentially expressed in denervated muscle atrophy. In this meta-analysis, we obtained 429 up-regulated genes, 525 down-regulated genes and a batch of key microRNAs in denervated muscle atrophy. We found eight important microRNA-mRNA interactions (miR-1/Jun, miR-1/Vegfa, miR-497/Vegfa, miR-23a/Vegfa, miR-206/Vegfa, miR-497/Suclg1, miR-27a/Suclg1, miR-27a/Mapk14). The top five KEGG pathways enriched by Den-genes are Insulin signaling pathway, T cell receptor signaling pathway, MAPK signaling pathway, Toll-like receptor signaling pathway and B cell receptor signaling pathway. Our research has delineated the RNA regulatory network of denervated muscle atrophy, and uncovered the specific genes and terms in denervated muscle atrophy.

scholarly journals Characterization of Long Non-coding RNA Profile in RD and SH-SY5Y Cells Infected by CV-B5 using RNA Sequencing

2021 ◽  
Author(s):  
Wei Chen ◽  
Peiying Teng ◽  
Heng Yang ◽  
Jing Li ◽  
Fan Yang
Keyword(s):  
Signaling Pathway ◽  
Rna Sequencing ◽  
Expression Profiles ◽  
Wnt Signaling Pathway ◽  
Foot And Mouth Disease ◽  
Differentially Expressed ◽  
Host Interactions ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Hand, foot, and mouth disease caused by Coxsackievirus B5 (CV-B5) poses considerable threats to the health of infants especially in neurological damage. And the long noncoding RNAs (lncRNAs) act pivotal factors in regulating and participating in virus-host interactions. However, the role of lncRNAs in CV-B5-host interactions has not yet been elucidated. In this study, we used the RNA sequencing to determine the expression profiles of lncRNAs in CV-B5 infected human rhabdomyosarcoma (RD) and SH-SY5Y cells. Our results identified that in the differentially expressed lncRNAs a total of 508 up-regulated and 760 down-regulated lncRNAs in RD cell, with 46.2% were lincRNAs, 28.6% were anti-sense lncRNAs, 24.1% were sense overlapping lncRNAs, and 1.0% were sense intronic lncRNAs. Moreover, 792 lncRNAs were significantly increased and 811 lncRNAs were greatly decreased in SH-SY5Y cell including 48.6% were lincRNAs, 34.7% were anti-sense lncRNAs, 16.0% were sense overlapping lncRNAs, and 0.8% were sense intronic lncRNAs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway showed that the differentially expressed lncRNAs participated in the occurrence of disease in RD cell and associated with signaling pathway in SH-SY5Y cell after CVB5 infection respectively. In addition, similar results were obtained when seven lncRNAs were selected for validation using RT-qPCR assays. Moreover, we conducted the candidate lncRNA-IL12A secondary structures and found that it inhibits viral replication through Wnt signaling pathway. Our results reveal that lncRNAs can become a possible novel molecular target for the prevention and treatment of CV-B5 infection, and provided information for distinguishing neurogenic CV-B5 disease.

scholarly journals Screening for differentially expressed circRNAs in ischemic stroke by RNA sequencing

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Duncan Wei ◽  
Jian Chen ◽  
Xiaopu Chen ◽  
Shaoyan Wu ◽  
Zhaolin Chen ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Rna Sequencing ◽  
Cell Receptor ◽  
Differentially Expressed ◽  
Receptor Signaling ◽  
Qrt Pcr ◽  
Receptor Signaling Pathway ◽  
Cell Receptor Signaling ◽  
Host Genes

Abstract Background Ischemic stroke is a disease with high rate of death and disability worldwide. CircRNAs, as a novel type of non-coding RNAs, lacking 5’ caps and 3’ poly-A tails, has been associated with ischemic stroke. This study aimed to investigate key circRNAs related to ischemic stroke. Methods RNA sequencing was performed obtain the circRNA expression profiles from peripheral whole blood of three ischemic stroke patients and three healthy individuals. Through bioinformatic analysis, differentially expressed circRNAs (DEcircRNAs) were identified, and GO and pathway analyses for the host genes of DEcircRNAs were conducted. The expression levels of selected circRNAs were analyzed with qRT-PCR. To further explore the functions of key circRNAs, a DEcircRNA-miRNA interaction network was constructed. Results A total of 736 DEcircRNAs were detected in ischemic stroke. Functional annotation of host genes of DEcircRNAs revealed several significantly enriched pathways, including Fc epsilon RI signaling pathway, B cell receptor signaling pathway, and T cell receptor signaling pathway. The qRT-PCR results were largely in keeping with our RNA-seq data. The ROC curve analyses indicated that hsa_circ_0000745, hsa_circ_0001459, hsa_circ_0003694 and hsa_circ_0007706 with relatively high diagnostic value. A circRNA-miRNA network, including 1544 circRNA-miRNA pairs, 456 circRNAs and 4 miRNAs, was obtained. Conclusions The results of our study may help to elucidate the specific mechanism underlying ischemic stroke.

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