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Identification of specific lncRNA signatures in breast cancer (BC)

ABSTRACT: In order to develop novel biomarkers in breast cancer, we applied a competing endogenous RNA (ceRNA) microarray to identify differentially expressed lncRNAs in BC tissue.

ORGANISM(S): Homo sapiens

PROVIDER: GSE156229 | GEO | 2020/08/14

REPOSITORIES: GEO

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Identification of specific ceRNA signatures in prostate cancer (PCa)

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Identification of exosomal mRNA, lncRNA and circRNA signatures in an osteoarthritis synovial fluid-exosomal study

Project description:Aims Osteoarthritis (OA) is a common degenerative disease that is pathologically characterized by destruction of the joint matrix and reduction of articular chondrocytes, resulting in joint deformity and motor dysfunction. However, the molecular mechanisms governing this pathology have not been fully elucidated to date. Methods In this study, we determined the expression levels of lncRNAs, circRNAs, and mRNAs extracted from synovial exosomes of OA and control patients. A network of circRNA/lncRNA–miRNA–mRNA interactions was established using MiRanda and TargetScan software to explore OA pathogenesis. The exosomal lncRNA, circRNA and mRNA expression profiles of the OA and control groups were analysed using LC human competing endogenous RNA (ceRNA) microarrays. The differentially expressed genes were identified to determine their potential roles in the pathogenesis of OA by bioinformatic analysis. Results Compared with the control group, 11 mRNAs, 52 lncRNAs, and 30 circRNAs were upregulated, while 41 mRNAs, 144 lncRNAs, and 68 circRNAs were downregulated in osteoarthritis synovial exosomes. The final ceRNA network of lncRNAs and circRNAs exhibited a complex interaction between ncRNA and mRNA related to OA pathological mechanisms. An intersection analysis of the ceRNA network showed that 22 miRNAs, 45 lncRNAs, and 34 circRNAs in the PI3K/Akt and autophagy pathways correlated with 7 enriched mRNAs and may play important roles in OA pathological mechanisms. Conclusion Our work analysed mRNA/lncRNA/circRNA expression and displayed the ceRNA network of lncRNAs and circRNAs to profile the pathogenesis of OA in synovial exosomes. The results of this study may help to elucidate the pathogenesis of OA and may provide important references for further research attempting to identify more effective targets for the diagnosis and therapy of OA.

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Integrative analysis of differential circular RNA and long noncoding RNA profiles and associated competing endogenous RNA networks in esophageal squamous cell carcinoma

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Transcriptomic analysis and competing endogenous RNA network in the human endometrium between proliferative and mid-secretory phases

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A Competing Endogenous RNA Network in Circulating Extracellular Vesicles Reveals Differentially-expressed Functional lncRNA in Human Subjects with Metabolic Syndrome

Project description:The metabolic syndrome (MetS), a collective cluster of disease risk factors that includes dyslipidemia, obesity, inflammation, hypertension, and insulin resistance, affects numerous people worldwide. Accumulating studies have shown that long-noncoding RNAs (lncRNA) serve as competing endogenous RNA (ceRNA) to play essential roles in regulating gene expression in various diseases. To explore the role of lncRNAs as ceRNAs in MetS, we examined a MetS-associated network in circulating extracellular vesicles (EVs) collected from systemic blood of MetS and control patients (n=5 each). MetS patients showed elevated body-weight, glucose, blood pressure, insulin, liver injury and inflammatory markers levels. In total, 191 differentially-expressed (DE) lncRNAs, 1389 mRNAs, and 138 miRNAs were selected for further analysis. Biological processes and pathway functional enrichment analysis were performed based on the Database for Annotation, Visualization, and Integrated Discovery (DAVID) database. LncRNA/mRNA/miRNA ceRNA network was constructed by Cytoscape v3.8 based on the DE-RNAs, and included 13 lncRNAs, 8 miRNAs, and 64 mRNAs. We found that the lncRNA-associated ceRNA network members potentially serve as regulators of central cellular processes and complications of MetS, including cancer. These findings suggest that MetS alters the interactions among the ceRNA network components in circulating EV-specific ceRNA network, and implicate the cargo of circulating EVs in ramifications of MetS.

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Comprehensive analysis of the whole coding and noncoding RNA transcriptome expression profiles and construction of the circRNA-lncRNA co-regulated ceRNA network in laryngeal squamous cell carcinoma [lncRNA-mRNA]

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Long non-coding RNA HOTTIP promotes CCL3 expression and induces cartilage degradation by sponging miR-455-3p

Project description:Long non-coding RNAs (lncRNAs) play pivotal roles in diseases such as osteoarthritis (OA). However, knowledge of the biological roles of lncRNAs is limited in OA. We aimed to explore the biological function and molecular mechanism of HOTTIP in chondrogenesis and cartilage degradation. We used the human mesenchymal stem cell (MSC) model of chondrogenesis, in parallel with, tissue biopsies from normal and OA cartilage to detect HOTTIP, CCL3, and miR-455-3p expression in vitro. Biological interactions between HOTTIP and miR-455-3p were determined by RNA silencing and overexpression in vitro. We evaluated the effect of HOTTIP on chondrogenesis and degeneration, and its regulation of miR-455-3p via competing endogenous RNA (ceRNA). Our in vitro ceRNA findings were further confirmed within animal models in vivo. Mechanisms of ceRNAs were determined by bioinformatic analysis, a luciferase reporter system, RNA pull-down, and RNA immunoprecipitation (RIP) assays. We found reduced miR-455-3p expression and significantly upregulated lncRNA HOTTIP and CCL3 expression in OA cartilage tissues and chondrocytes. The expression of HOTTIP and CCL3 was increased in chondrocytes treated with interleukin-1β (IL-1β) in vitro. Knockdown of HOTTIP promoted cartilage-specific gene expression and suppressed CCL3. Conversely, HOTTIP overexpression reduced cartilage-specific genes and increased CCL3. Notably, HOTTIP negatively regulated miR-455-3p and increased CCL3 levels in human primary chondrocytes. Mechanistic investigations indicated that HOTTIP functioned as ceRNA for miR-455-3p enhanced CCL3 expression. Taken together, the ceRNA regulatory network of HOTTIP/miR-455-3p/CCL3 plays a critical role in OA pathogenesis and suggests HOTTIP is a potential target in OA therapy.

2019-08-12 | PXD014988 | Pride

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