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RNA Dysregulation in Human Diseases: from Basic to Translational Applications

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 2929

Special Issue Editor

1. Division of Cancer Biology, Research Institute, National Cancer Center, Goyang 10408, Korea
2. Department of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea
Interests: RNA-binding proteins; RNA modifiers; oncogenic RNAs; noncoding RNA; miRNAs; posttranscriptional regulation; cancer

Special Issue Information

Dear Colleagues,

RNA molecules undergo multiple posttranscriptional processes for gene expression regulation in eukaryotes, including RNA splicing, transport, localization, stability, translation, and degradation. Recent reports have shown various examples of the dysregulation of RNA-linked biological processes in major human diseases. This Special Issue aims to understand, diagnose, and develop therapeutic approaches for the regulation of RNA-mediated biological processes during tumorigenesis, development of genetic disorder, and RNA virus infection in humans.

This issue will handle the following RNA-related research areas:

  1. Role of RNA post-transcriptional regulome (RNA-binding proteins, RNA modifiers, and modulatory RNAs) in cancer, and their molecular interplay with microRNAs and other oncogenic RNAs;
  2. Molecular interplay between host cellular RNA regulome and RNA viruses during the virus-mediated pathogenesis in humans;
  3. Molecular interplay between RNA and RNA regulome for the dysregulation of splicing in human diseases;
  4. Diagnostic application of microRNA, development of microRNA-sensing system, and its translational application in cancer;
  5. Extracellular small noncoding RNA in cancer malignancy; basic, diagnostic and translational applications.

Prof. Dr. Jong Heon Kim
Guest Editor

Manuscript Submission Information

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Keywords

  • Post-transcriptional regulation;
  • RNA-binding proteins;
  • RNA modifiers;
  • Noncoding RNAs;
  • MicroRNAs;
  • Cancer;
  • Oncogenic RNAs;
  • Regulation of splicing;
  • RNA viruses;
  • Extracellular small noncoding RNAs.

Published Papers (1 paper)

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Research

20 pages, 4192 KiB  
Article
Regulation of Survival Motor Neuron Gene Expression by Calcium Signaling
by Kwangman Choi, Ansook Yang, Jiyeon Baek, Hyejeong Jeong, Yura Kang, Woosun Baek, Joon-Chul Kim, Mingu Kang, Miri Choi, Youngwook Ham, Min-Jeong Son, Sang-Bae Han, Janghwan Kim, Jae-Hyuk Jang, Jong Seog Ahn, Haihong Shen, Sun-Hee Woo, Jong Heon Kim and Sungchan Cho
Int. J. Mol. Sci. 2021, 22(19), 10234; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910234 - 23 Sep 2021
Viewed by 2522
Abstract
Spinal muscular atrophy (SMA) is caused by homozygous survival of motor neurons 1 (SMN1) gene deletion, leaving a duplicate gene, SMN2, as the sole source of SMN protein. However, a defect in SMN2 splicing, involving exon 7 skipping, results in [...] Read more.
Spinal muscular atrophy (SMA) is caused by homozygous survival of motor neurons 1 (SMN1) gene deletion, leaving a duplicate gene, SMN2, as the sole source of SMN protein. However, a defect in SMN2 splicing, involving exon 7 skipping, results in a low level of functional SMN protein. Therefore, the upregulation of SMN protein expression from the SMN2 gene is generally considered to be one of the best therapeutic strategies to treat SMA. Most of the SMA drug discovery is based on synthetic compounds, and very few natural compounds have been explored thus far. Here, we performed an unbiased mechanism-independent and image-based screen of a library of microbial metabolites in SMA fibroblasts using an SMN-specific immunoassay. In doing so, we identified brefeldin A (BFA), a well-known inhibitor of ER-Golgi protein trafficking, as a strong inducer of SMN protein. The profound increase in SMN protein was attributed to, in part, the rescue of the SMN2 pre-mRNA splicing defect. Intriguingly, BFA increased the intracellular calcium concentration, and the BFA-induced exon 7 inclusion of SMN2 splicing, was abrogated by the depletion of intracellular calcium and by the pharmacological inhibition of calcium/calmodulin-dependent kinases (CaMKs). Moreover, BFA considerably reduced the expression of Tra2-β and SRSF9 proteins in SMA fibroblasts and enhanced the binding of PSF and hnRNP M to an exonic splicing enhancer (ESE) of exon 7. Together, our results demonstrate a significant role for calcium and its signaling on the regulation of SMN splicing, probably through modulating the expression/activity of splicing factors. Full article
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