Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.26.9 (ribonuclease)
 6,589 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

MicroRNAs have been reported to be stably detectable in plasma/serum and to exhibit resistance to endogenous ribonuclease activity because of binding to proteins such as Argonaute-2 and high-density lipoprotein, or being packed by secretory particles such as exosomes. These secretory particles include specific microRNAs and can function as intercellular transmitters. These findings could open-up a new and promising field in the use of circulating microRNAs for cancer treatment. In particular, miR-18a, which is located in the potentially oncogenic miR-17-92 cluster, is a highly expressed microRNAs in several types of cancers. The concentration of miR-18a in plasma/serum of patients with cancer such as esophageal (AUC=0.944), pancreatic (AUC=0.936), hepatocellular (AUC=0.881), colorectal and other types of cancers is much higher than that of healthy volunteers. Such reports provide evidence that circulating miR-18 might be a next-generation biomarker and contribute to cancer screening in non-invasive liquid biopsy, to a clinically-satisfactory degree of sensitivity and specificity.
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PMID:Circulating miR-18a: a sensitive cancer screening biomarker in human cancer. 2481 29

mRNA deadenylation is under the control of cis-acting regulatory elements, which include AU-rich elements (AREs) and microRNA (miRNA) targeting sites, within the 3' untranslated region (3' UTRs) of eukaryotic mRNAs. Deadenylases promote miRNA-induced mRNA decay through their interaction with miRNA-induced silencing complex (miRISC). However, the role of poly(A) specific ribonuclease (PARN) deadenylase in miRNA-dependent mRNA degradation has not been elucidated. Here, we present evidence that not only ARE- but also miRNA-mediated pathways are involved in PARN-mediated regulation of the steady state levels of TP53 mRNA, which encodes the tumor suppressor p53. Supporting this, Argonaute-2 (Ago-2), the core component of miRISC, can coexist in complexes with PARN resulting in the activation of its deadenylase activity. PARN regulates TP53 mRNA stability through not only an ARE but also an adjacent miR-504/miR-125b-targeting site in the 3' UTR. More importantly, we found that miR-125b-loaded miRISC contributes to the specific recruitment of PARN to TP53 mRNA, and that can be reverted by the ARE-binding protein HuR. Together, our studies provide new insights into the role of PARN in miRNA-dependent control of mRNA decay and into the mechanisms behind the regulation of p53 expression.
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PMID:PARN deadenylase is involved in miRNA-dependent degradation of TP53 mRNA in mammalian cells. 2640 Jan 60