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Small noncoding RNAs as biomarkers for pregnancy complications
Published in Moshe Hod, Vincenzo Berghella, Mary E. D'Alton, Gian Carlo Di Renzo, Eduard Gratacós, Vassilios Fanos, New Technologies and Perinatal Medicine, 2019
Liron Yoffe, Meitar Grad, Avital Luba Polsky, Moshe Hod, Noam Shomron
miRNAs are an abundant class of small (∼22 nucleotides) ncRNAs that are estimated to downregulate the expression of more than 60% of protein-coding genes (6,9). miRNAs play pivotal post-transcriptional regulatory roles in various physiological functions. They bind messenger RNAs (mRNAs) at their 3′ untranslated region (UTR) and initiate either the mRNA degradation or translational repression (9,10). miRNAs are transcribed by RNA polymerase II from either specific miRNA gene loci or through splicing of mirtrons between exons of a host gene (6,9,11,12). Both transcription processes result in the formation of primary miRNAs (pri-miRNAs) that are processed by ribonuclease III (RNase III) enzymes Drosha and Dicer (along with other enzymes and aiding proteins) to form precursor miRNAs (pre-miRNAs) and then mature miRNAs (6,9,11,12). Mature miRNAs are then loaded into the RNA-induced silencing complex (RISC) to downregulate mRNA translation (6,9,11,12). A single miRNA can regulate tens to hundreds of downstream genes from a wide spectrum of biological pathways (13) and may also interact with other miRNAs to regulate gene expression (6). Thus, some miRNAs can be considered master regulators of various biological processes, such as cell proliferation, differentiation, apoptosis, and development (6,9).
Vascular endothelial growth factor C promotes cervical cancer cell invasiveness via regulation of microRNA-326/cortactin expression
Published in Gynecological Endocrinology, 2018
Yang Cheng, Shuyi Jiang, Jin Yuan, Junxiu Liu, Tommaso Simoncini
The mechanism underlying miR-326 expression regulated by VEGF-C is unknown. In our study, c-Src inhibitor or siRNA inhibited VEGF-C effect on miR-326 expression, indicating that c-Src is an important signaling in this event. Actually, c-Src is the tyrosine kinase that modulates the actin cytoskeleton and cell adhesions through the concerted action of their protein-interaction and kinase domains [25]. Interestingly, it was reported that c-Src is the upstream of cortactin [26]. From this point of view, our findings provided the new mechanistic explanation that c-Src regulates cortactin via miR-326. c-Src signalings are fine-tuned by microRNAs [27]. However, currently it is not clear that how c-Src regulates miR-326 expression. miR-326 is an intragenic miRNA, possibly a mirtron as its genetic locus is in the first intron of its host gene Arrestin β1 (ARRB1). It was reported that c-Src was capable of regulating arrestin β1 expression. Therefore, it would be possible that c-Src regulates some transcription factor that bind to the promoter of Arrestin β1 gene and consequently alters miR-326 expression. This, however, is currently under our investigation.
Advances in the understanding of hereditary ataxia – implications for future patients
Published in Expert Opinion on Orphan Drugs, 2018
Anna Zeitlberger, Heather Ging, Suran Nethisinghe, Paola Giunti
RNAi is a naturally occurring post-transcriptional gene suppression process, which functions through noncoding double-stranded RNA sequences. RNAi effectors can be introduced into the cell in the form of short-interfering RNAs, short hairpin RNAs or artificial miRNAs [131]. Both non-allele-specific and allele-specific RNAi approaches have demonstrated improvement on disease and molecular phenotype in SCA7 [132,133] and SCA3 [134,135] rodent models. Most recently, combined gene-knockdown-replacement therapy using mirtrons has been explored in fibroblast cell lines from SCA7 patients [136].
Emerging roles of noncoding RNAs in T cell differentiation and functions in autoimmune diseases
Published in International Reviews of Immunology, 2019
Additional, non-canonical pathway for the biogenesis of miRNAs was also reported in Caenorhabditis elegans, Drosophila melanogaster and mammals, which is Drosha-independent. In this pathway, short-hairpin introns are spliced out by spliceosome into “pre-miRNA” known as “mirtrons”. However, this is an uncommon pathway for miRNA biogenesis and majority of miRNA are generated by Drosha-dependent cleavage pathway [63, 64].