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microarray的相关文献在2001年到2023年内共计114篇,主要集中在肿瘤学、内科学、基础医学 等领域,其中期刊论文112篇、会议论文2篇、相关期刊51种,包括国际肝胆胰疾病杂志(英文版)、中国科学、世界胃肠病学杂志:英文版等; 相关会议2种,包括第四届海峡两岸土壤及地下水污染与整治研讨会、2004年肝病实验室诊断与临床研究专题学术会议等;microarray的相关文献由555位作者贡献,包括Fusako Mitsunaga、Shin Nakamura、Hiromasa Yoshie等。

microarray—发文量

期刊论文>

论文:112 占比:98.25%

会议论文>

论文:2 占比:1.75%

总计:114篇

microarray—发文趋势图

microarray

-研究学者

  • Fusako Mitsunaga
  • Shin Nakamura
  • Hiromasa Yoshie
  • Hong-Sig Sin
  • Jia Yang
  • Kathleen M. Eyster
  • Ki-Chan Ha
  • Seung-Hwan Jang
  • Soo-Wan Chae
  • Su-Jin Jung
  • 期刊论文
  • 会议论文

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    • Bin Pan; Di Guo; Li Jing; Ke Li; Xin Li; Gen Li; Xiao Gao; Zhi-Wen Li; Wei Zhao; Hu Feng; Meng-Han Cao
    • 摘要: Research has shown that long-chain noncoding RNAs(lncRNAs) are involved in the regulation of a variety of biological processes, including peripheral nerve regeneration, in part by acting as competing endogenous RNAs. c-Jun plays a key role in the repair of peripheral nerve injury. However, the precise underlying mechanism of c-Jun remains unclear. In this study, we performed microarray and bioinformatics analysis of mouse crush-injured sciatic nerves and found that the lncRNA Pvt1 was overexpressed in Schwann cells after peripheral nerve injury. Mechanistic studies revealed that Pvt1 increased c-Jun expression through sponging miRNA-214. We overexpressed Pvt1 in Schwann cells cultured in vitro and found that the proliferation and migration of Schwann cells were enhanced, and overexpression of miRNA-214 counteracted the effects of Pvt1 overexpression on Schwann cell proliferation and migration. We conducted in vivo analyses and injected Schwann cells overexpressing Pvt1 into injured sciatic nerves of mice. Schwann cells overexpressing Pvt1 enhanced the regeneration of injured sciatic nerves following peripheral nerve injury and the locomotor function of mice was improved. Our findings reveal the role of lncRNAs in the repair of peripheral nerve injury and highlight lncRNA Pvt1 as a novel potential treatment target for peripheral nerve injury.
    • Jia Yang; Yueyang Yu; Zhengze Zhang; Bo Su; Yun Zheng; Yang Liu
    • 摘要: MicroRNAs (miRNAs) are a functional small non-coding RNA and play essential roles in gene regulation indevelopment, differentiation and proliferation. In order to investigate the miRNAs function in Lewis rat hippocampal development, in this study, newborn and adult hippocampi were deliberately selected to analyze the miRNA expression profiles by microarray. Microarray analyses identified 22 differentially expressed miRNAs (>1.5 fold, intersection of two sets). Of these, 12 were down-regulated and 10 were up-regulated during hippocampus development. DAVID Functional Annotation Cluster (FAC) analysis of the 317 predicted target genes of down-regulated miRNAs revealed confident enrichment scores for cell adhesion and neuron development etc., indicating the functional significance and importance of these miRNAs during hippocampal development. Bioinformatic analyses of the differentially expressed miRNAs have identified a number of miRNAs with putative involvement in the hippocampus developing process. This study lays a solid foundation for further studies to clarify the important regulation function of miRNAs in brain tissue.
    • Monia Cecati; Matteo Giulietti; Alessandra Righetti; Berina Sabanovic; Francesco Piva
    • 摘要: BACKGROUND Pancreatic ductal adenocarcinoma(PDAC)is the fourth leading cause of death among cancers,it is characterized by poor prognosis and strong chemoresistance.In the PDAC microenvironment,stromal cells release different extracellular components,including CXCL12.The CXCL12 is a chemokine promoting the communication between tumour and stromal cells.Six different splicing isoforms of CXCL12 are known(α,β,γ,δ,ε,θ)but their role in PDAC has not yet been characterized.AIM To investigate the specific role ofα,β,andγCXCL12 isoforms in PDAC onset.METHODS We used hTERT-HPNE E6/E7/KRasG12D(Human Pancreatic Nestin-Expressing)cell line as a pancreatic pre-tumour model and exposed it to theα,β,andγCXCL12 isoforms.The altered expression profiles were assessed by microarray analyses and confirmed by Real-Time polymerase chain reaction.The functional enrichment analyses have been performed by Enrichr tool to highlight Gene Ontology enriched terms.In addition,wound healing assays have been carried out to assess the phenotypic changes,in terms of migration ability,induced by theα,β,andγCXCL12 isoforms.RESULTS Microarray analysis of hTERT-HPNE cells treated with the three different CXCL12 isoforms highlighted that the expression of only a few genes was altered.Moreover,theαandβisoforms showed an alteration in expression of different genes,whereasγisoform affected the expression of genes also common withαandβisoforms.Theβisoform altered the expression of genes mainly involved in cell cycle regulation.In addition,all isoforms affected the expression of genes assay confirmed that CXCL12 enhanced the migration ability of hTERT-HPNE cells.Among the CXCL12 splicing isoforms,theγisoform showed higher induction of migration thanαandβisoforms.CONCLUSION Our data suggests an involvement and different roles of CXCL12 isoforms in PDAC onset.However,more investigations are needed to confirm these preliminary observations.
    • Bo-Zhao Ma
    • 摘要: Background:CD4+CD25+Foxp3+regulatory T cells are essential for immune homeostasis.Naive Treg cells can undergo further differentiation into an effector state in response to antigen and a variety of environment cues.However,the potent mechanisms are poorly understood.Autophagy maybe one of the potent mechanisms participate in the differentiation process.Methods:The gene expression profiles of GSE72494 were downloaded from Gene Expression Omnibus database and differently expressed genes were filtered by EdgeR package and R.TIGIT+Treg and TIGIT-Treg cells were separated by magnetic beads and flow cytometry.RT-PCR was used to determine the mRNA level and the protein expression of autophagy-related proteins was determined by western blot assay.Results:In total,1,896 DEGs were identified between TIGIT+and TIGIT-Treg cells,including 1,280 up-regulated genes and 616 down-regulated genes.Three autophagy related genes,MAP1LC3A(LC3),SQSTM1(P62)and BECN1(Beclin1)were increased in TIGIT+Treg cells.Mechanistic target of rapamycin,a key molecule may have the function of inhibiting autophagy was down-regulated in TIGIT+Treg cells.Autophagy-related proteins LC3,P62 and Beclin1 were significantly increased and the expression of mTOR was significantly decreased in TIGIT+Treg cells.Conclusion:TIGIT+Treg cell is a subset of Treg cells with unique functions.Autophagy-related processes may be involved in the differentiation of TIGIT-Treg into TIGIT+Treg cells.Inducing the generation of TIGIT+effect Tregs may be a new way to prevent the immune rejection of acute organ transplantation.
    • Somsak Likhitrattanapisal; Supeecha Kumkate; Pravech Ajawatanawong; Kanokpan Wongprasert; Rutaiwan Tohtong; Tavan Janvilisri
    • 摘要: BACKGROUND In the past decades,the potential of microRNA(miRNA)in cancer diagnostics and prognostics has gained a lot of interests.In this study,a meta-analysis was conducted upon the pooled miRNA microarray data of cholangiocarcinoma(CCA).AIM To identify differentially expressed(DE)miRNAs and perform functional analyses in order to gain insights to understanding miRNA-target interactions involved in tumorigenesis pathways of CCA.METHODS Raw data from 8 CCA miRNA microarray datasets,consisting of 443 samples in total,were integrated and statistically analyzed to identify DE miRNAs via comparison of levels of miRNA expression between CCA and normal bile duct samples using t-tests(P<0.001).The 10-fold cross validation was performed in order to increase the robustness of the t-test results.Our data showed 70 up-regulated and 48 down-regulated miRNAs in CCA. GeneOntology and pathway enrichment analyses revealed that mRNA targets of DEmiRNAs were significantly involved in several biological processes. The mostprominent dysregulated pathways included phosphatidylinositol-3 kinases/Akt,mitogen-activated protein kinase and Ras signaling pathways.CONCLUSIONDE miRNAs found in our meta-analysis revealed dysregulation in major cancerpathways involved in the development of CCA. These results indicated thenecessity of understanding the miRNA-target interactions and the significance ofdysregulated miRNAs in terms of diagnostics and prognostics of cancers.
    • Na Li; Rui-Hua Shi
    • 摘要: BACKGROUND Statistics indicate that the incidence of Crohn’s disease(CD)is rising in many countries.The poor understanding on the pathological mechanism has limited the development of effective therapy against this disease.Previous studies showed that long noncoding RNAs(lncRNAs)could be involved in autoimmune diseases including CD,but the detailed molecular mechanisms remain unclear.AIM To identify the differentially expressed lncRNAs in the intestinal mucosa associated with CD,and to characterize their pathogenic role(s)and related mechanisms.METHODS The differential expression of lncRNAs was screened by high-throughput RNA sequencing,and the top candidate genes were validated in an expanded cohort by real-time PCR.The regulatory network was predicted by bioinformatic software and competitive endogenous RNA analysis,and was characterized in Caco-2 and HT-29 cell culture using methods of cell transfection,real-time PCR,Western blotting analysis,flow cytometry,and cell migration and invasion assays.Finally,these findings were confirmed in vivo using a CD animal model.RESULTS The 3'end of lncRNACNN3-206 and the 3’UTR of Caspase10 contain highaffinity miR212 binding sites.lncRNACNN3-206 expression was found to be significantly increased in intestinal lesions of CD patients.Activation of the lncRNACNN3-206-miR-212-Caspase10 regulatory network led to increased apoptosis,migration and invasion in intestinal epithelial cells.Knockdown of lncRNACNN3-206 expression alleviated intestinal mucosal inflammation and tissue damage in the CD mouse model.CONCLUSION lncRNACNN3-206 may play a key role in CD pathogenesis.lncRNACNN3-206 could be a therapeutic target for CD treatment.
    • Yao-Yao Bian; Li-Li Yang; Bin Zhang; Wen Li; Zheng-Jun Li; Wen-Lin Li; Li Zeng
    • 摘要: BACKGROUND Post-traumatic stress disorder(PTSD)is a serious stress-related disorder.AIM To identify the key genes and pathways to uncover the potential mechanisms of PTSD using bioinformatics methods.METHODS Gene expression profiles were obtained from the Gene Expression Omnibus database.The differentially expressed genes(DEGs)were identified by using GEO2R.Gene functional annotation and pathway enrichment were then conducted.The gene-pathway network was constructed with Cytoscape software.Quantitative real-time polymerase chain reaction(qRT-PCR)analysis was applied for validation,and text mining by Coremine Medical was used to confirm the connections among genes and pathways.RESULTS We identified 973 DEGs including 358 upregulated genes and 615 downregulated genes in PTSD.A group of centrality hub genes and significantly enriched pathways(MAPK,Ras,and ErbB signaling pathways)were identified by using gene functional assignment and enrichment analyses.Six genes(KRAS,EGFR,NFKB1,FGF12,PRKCA,and RAF1)were selected to validate using qRT-PCR.The results of text mining further confirmed the correlation among hub genes and the enriched pathways.It indicated that these altered genes displayed functional roles in PTSD via these pathways,which might serve as key signatures in the pathogenesis of PTSD.CONCLUSION The current study identified a panel of candidate genes and important pathways,which might help us deepen our understanding of the underlying mechanism of PTSD at the molecular level.However,further studies are warranted to discover the critical regulatory mechanism of these genes via relevant pathways in PTSD.
    • Jing Lv; Lei Guo; Ji-Han Wang; Yu-Zhu Yan; Jun Zhang; Yang-Yang Wang; Yan Yu; Yun-Fei Huang; He-Ping Zhao
    • 摘要: BACKGROUND Esophageal adenocarcinoma(EAC) is an aggressive disease with high mortality and an overall 5-year survival rate of less than 20%. Barrett's esophagus(BE) is the only known precursor of EAC, and patients with BE have a persistent and excessive risk of EAC over time. Individuals with BE are up to 30-125 times more likely to develop EAC than the general population. Thus, early detection of EAC and BE could significantly improve the 5-year survival rate of EAC. Due to the limitations of endoscopic surveillance and the lack of clinical risk stratification strategies, molecular biomarkers should be considered and thoroughly investigated.AIM To explore the transcriptome changes in the progression from normal esophagus(NE) to BE and EAC.METHODS Two datasets from the Gene Expression Omnibus(GEO) in NCBI Database(https://www.ncbi.nlm.nih.gov/geo/) were retrieved and used as a training and a test dataset separately, since NE, BE, and EAC samples were included and the sample sizes were adequate. This study identified differentially expressed genes(DEGs) using the R/Bioconductor project and constructed trans-regulatory networks based on the Transcriptional Regulatory Element Database and Cytoscape software. Enrichment of Kyoto Encyclopedia of Genes and Genomes(KEGG) and Gene Ontology(GO) terms was identified using the Database for Annotation, Visualization, and Integrated Discovery(DAVID) Bioinformatics Resources. The diagnostic potential of certain DEGs was assessed in both datasets.RESULTS In the GSE1420 dataset, the number of up-regulated DEGs was larger than that of down-regulated DEGs when comparing EAC vs NE and BE vs NE. Among these DEGs, five differentially expressed transcription factors(DETFs) displayed the same trend in expression across all the comparison groups. Of these five DETFs,E2 F3, FOXA2, and HOXB7 were up-regulated, while PAX9 and TFAP2 C were down-regulated. Additionally, the majority of the DEGs in trans-regulatory networks were up-regulated. The intersection of these potential DEGs displayed the same direction of changes in expression when comparing the DEGs in the GSE26886 dataset to the DEGs in trans-regulatory networks above. The receiver operating characteristic curve analysis was performed for both datasets and found that TIMP1 and COL1 A1 could discriminate EAC from NE tissue, while REG1 A, MMP1, and CA2 could distinguish BE from NE tissue. DAVID annotation indicated that COL1 A1 and MMP1 could be potent biomarkers for EAC and BE, respectively, since they participate in the majority of the enriched KEGG and GO terms that are important for inflammation and cancer.CONCLUSION After the construction and analyses of the trans-regulatory networks in EAC and BE, the results indicate that COL1 A1 and MMP1 could be potential biomarkers for EAC and BE, respectively.
    • Rui-Feng Qin; Jia Zhang; Hao-Ran Huo; Zeng-Jiang Yuan; Jia-Dong Xue
    • 摘要: BACKGROUND Pancreatic cancer is a deadly malignancy with aggressive properties. MicroRNAs (miRNAs) participate in the pathogenesis of a variety of diseases and molecular processes by targeting functional mRNAs. Nevertheless, the regulatory role of miRNAs in signaling pathways involved in pancreatic cancer remains largely unknown. AIM To explore the molecular regulation involved in pancreatic cancer and potential mechanisms of miR-205. METHODS Microarray analysis was performed to investigate the expression profile of miRNAs in pancreatic cancer. Expression of miR-205 was validated by qRT-PCR. Target prediction and functional enrichment analysis were employed to seek potential target genes of miR-205 and potential functions of these genes. The target binding of miR-205 and adenomatous polyposis coli (APC) was validated by luciferase reporter assay. APC protein expression in pancreatic cancer was validated by qRT-PCR and Western blot. Proliferation was evaluated by MTT and colony formation assays. RESULTS A large number of miRNAs with altered expression were identified in pancreatic cancer. MiR-205 was significantly up-regulated. APC was found to be a validated target of miR-205 and down-regulated in pancreatic cancer. Proliferation experiments showed that miR-205 could promote cell proliferation in pancreatic cancer by targeting APC. CONCLUSION The above findings suggested that miR-205 mediated APC regulation contributes to pancreatic cancer development, which could be considered as a novel prognostic biomarker for clinical care.
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