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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

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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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Cell-free lncRNA expression signatures in urine serve as novel noninvasive biomarkers for diagnosis and recurrence prediction of bladder cancer

Project description:To identify lncRNAs dysregulated in BC, we assessed the lncRNA expression profile in pooled urine samples of 10 BC patients and 10 controls by microarray. A total of 3093 lncRNAs determined differential expression (fold change>=2.0) between BC patients and controls. Among them, 1680 lncRNAs were up-regulated and 1413 lncRNAs were down-regulated in BC. Of all the differentially expressed lncRNAs indicated by lncRNA expression profiling, 26 lncRNAs (fold change>25) were firstly selected for further evaluation, in which 16 lncRNAs were up-regulated and 10 lncRNAs were down-regulated in BC.

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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

NACER, a liver-specific lncRNA, functions as Nrf2-activating competing endogenous RNA for Plk2 and p21cip1

Project description:LncRNA for anti-oxidative capacity control has not been discovered yet. Nrf2 is a central molecule for cellular defense by increasing anti-oxidative capacity. Here, we identified a novel lncRNA named ‘NACER’ (Nrf2 Activating Competing Endogenous RNA) transcribed from an upstream region of MIR122. NACER existed in the cytoplasm, suggestive of its function as competing endogenous RNA (ceRNA, miRNA sponge). NACER served as ceRNA for Plk2 and p21cip1 through binding for miR-128/224, inducing Plk2/Nrf2/p21cip1 complexation for Nrf2 activation in cells under p53-activating conditions (i.e., DNA damage and serum deprivation). NACER expression was suppressed when apoptosis was initiated, being a rheostat for cell fate determination. NACER levels correlated with the recurrence free survival rate of patients with hepatocellular carcinoma after surgery. Collectively, NACER promotes Plk2 and p21cip1 translation by competing for specific miRNAs, activating Nrf2 under the surviving condition from oxidative stress, implying that NACER plays a fine-tuning rheostat for cell fate decision.

2024-05-01 | GSE115409 | GEO

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