Biomarker Identification in Membranous Nephropathy Using a Long Non-coding RNA-Mediated Competitive Endogenous RNA Network

Increasing evidence indicates that paternal diet can result in metabolic changes in offspring, but the definite mechanism remains unclear in birds. Here, we fed breeder cocks five different diets containing 0, 0.25, 1.25, 2.50 and 5.00 mg kg −1 folate throughout life. Paternal folate supplementation (FS) was beneficial to the growth and organ development of broiler offspring. Most importantly, the lipid and glucose metabolism of breeder cocks and broiler offspring were affected by paternal FS, according to biochemical and metabolomic analyses. We further employed global analyses of hepatic and spermatozoal messenger RNA (mRNA), long non-coding RNA (lncRNA) and micro RNA (miRNA). Some key genes involved in the glycolysis or gluconeogenesis pathway and the PPAR signalling pathway, including PEPCK , ANGPTL4 and THRSP , were regulated by differentially expressed hepatic and spermatozoal miRNAs and lncRNAs in breeder cocks and broiler offspring. Moreover, the expression of ANGPTL4 could also be regulated by differentially expressed miRNAs and lncRNAs in spermatozoa via competitive endogenous RNA (ceRNA) mechanisms. Overall, this model suggests that paternal folate could transgenerationally regulate lipid and glucose metabolism in broiler offspring and the epigenetic transmission may involve altered spermatozoal miRNAs and lncRNAs.

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Identification of prognostic biomarkers in glioblastoma using a long non-coding RNA-mediated, competitive endogenous RNA network

Oncotarget ◽

10.18632/oncotarget.9569 ◽

2016 ◽

Vol 7 (27) ◽

pp. 41737-41747 ◽

Cited By ~ 24

Author(s):

Yuze Cao ◽

Peng Wang ◽

Shangwei Ning ◽

Wenbiao Xiao ◽

Bo Xiao ◽

...

Keyword(s):

Prognostic Biomarkers ◽

Non Coding Rna ◽

Long Non Coding Rna ◽

Competitive Endogenous Rna

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Long non-coding RNA HOTAIR functions as a competitive endogenous RNA to regulate PRAF2 expression by sponging miR-326 in cutaneous squamous cell carcinoma

Cancer Cell International ◽

10.1186/s12935-019-0992-x ◽

2019 ◽

Vol 19 (1) ◽

Cited By ~ 12

Author(s):

Guo-Jun Yu ◽

Yong Sun ◽

Da-Wei Zhang ◽

Peng Zhang

Keyword(s):

Cell Migration ◽

Cell Lines ◽

Cell Function ◽

Function Analysis ◽

Luciferase Reporter ◽

Luciferase Reporter Gene ◽

Non Coding Rna ◽

Cell Migration And Proliferation ◽

Long Non Coding Rna ◽

Competitive Endogenous Rna

Abstract Background LncRNAs may exert a regulatory effect in tumorigenesis. Although the expression of lncRNA HOTAIR has been confirmed to be notably elevated in the tissues of CSCC, its biological mechanism in CSCC is still unknown. Methods HOTAIR expression level in CSCC cell lines was monitored via qRT-PCR. Then CCK-8 assay, Transwell assay and EdU assay were adopted to detect cell migration and proliferation. Meanwhile, through bioinformatics analysis and luciferase reporter gene detection, a new target of HOTAIR was identified. Additionally, Western blotting and RIP analysis were adopted to discuss the possible mechanism. Results HOTAIR expression in CSCC cell lines exhibited an obvious elevation. Cell function analysis revealed that HOTAIR overexpression remarkably facilitated CSCC cell migration, proliferation and EMT process, which were impeded by down-regulation of HOTAIR. Furthermore, HOTAIR competitively bound to miR-326, so as to positively modulate miR-326 expression. Conclusions These results present that HOTAIR, as a ceRNA, regulates PRAF2 expression by competitive binding to miR-326 during CSCC.

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The long non-coding RNA TUG1-miR-9a-5p axis contributes to ischemic injuries by promoting cardiomyocyte apoptosis via targeting KLF5

Cell Death and Disease ◽

10.1038/s41419-019-2138-4 ◽

2019 ◽

Vol 10 (12) ◽

Cited By ~ 3

Author(s):

Di Yang ◽

Jie Yu ◽

Hui-Bin Liu ◽

Xiu-Qing Yan ◽

Juan Hu ◽

...

Keyword(s):

Myocardial Infarction ◽

Cardiomyocyte Apoptosis ◽

Luciferase Reporter ◽

Apoptotic Pathway ◽

Non Coding Rna ◽

Non Coding Rnas ◽

Long Non Coding Rna ◽

Cultured Cardiomyocytes ◽

Competitive Endogenous Rna ◽

Dual Luciferase Reporter Assay

AbstractNon-coding RNAs participate in many cardiac pathophysiological processes, including myocardial infarction (MI). Here we showed the interplay between long non-coding RNA taurine-upregulated gene 1 (lncR-TUG1), miR-9a-5p (miR-9) and Krüppel-like factor 5 (KLF5). LncR-TUG1 was upregulated in ischemic heart and in cultured cardiomyocytes exposed to H2O2. Knockdown of lncR-TUG1 markedly ameliorated impaired cardiac function of MI mice. Further study showed that lncR-TUG1 acted as a competitive endogenous RNA of miR-9, and silencing of lncR-TUG1 inhibited cardiomyocyte apoptosis by upregulating miR-9 expression. Furthermore, the miR-9 overexpression obviously prevented ischemia injury and significantly inhibited H2O2-induced cardiomyocyte apoptosis via inhibition of mitochondrial apoptotic pathway. KLF5, as a target gene of miR-9 by dual-luciferase reporter assay, was involved in the process of miR-9 in regulating cardiomyocyte apoptosis. Our data identified the KLF5 was downregulated by miR-9 overexpression and knockdown of KLF5 inhibited cardiomyocyte apoptosis induced by H2O2. MiR-9 exerts anti-cardiomyocyte apoptotic affects by targeting KLF5. Collectively, our data identify a novel function of lncR-TUG1/miR-9/KLF5 axis in regulating cardiomyocyte apoptosis that affects myocardial infarction progression.

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