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Small Non-coding RNAs in Normal Physiology, Development and Diseases
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Small Non-coding RNAs in Normal Physiology, Development and Diseases

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (25 November 2023) | Viewed by 4689

Special Issue Editors

Dr. Chen Chu

E-Mail Website
Guest Editor
Dana-Farber Cancer Institute, Boston, MA, USA
Interests: small non-coding RNA; reproduction; cancer; genetics
Dr. Lantao Gou

E-Mail Website
Guest Editor
Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai 200031, China
Interests: regulatory RNA; RNA and chromatin biology; reproduction and infertility

Special Issue Information

Dear Colleagues,

Small non-coding RNAs are a rapidly expanding family that play key regulatory roles in shaping various cellular activities, including development, normal physiology and diseases. Since their discovery in 1993, a significant number of small non-coding RNA classes have been identified, such as microRNAs (miRNAs), PIWI-interacting RNAs (piRNAs) and small non-coding RNAs, that are derived from tRNAs and rRNAs. The applications of high-throughput approaches have made great contributions to the discovery of new small non-coding RNAs in different species, tissues and cell types, and have aided in profiling small non-coding RNA dynamics in various biological/pathological processes. This Special Issue, “Small Non-coding RNAs in normal physiology, development and diseases”, aims to provide readers with recent advances in small non-coding RNA research. We welcome comprehensive reviews and original research manuscripts covering topics including, but not limited to, the discovery of new small non-coding RNA species, and  research on the functions and mechanisms of small non-coding RNAs in regulating normal physiological processes, development and diseases.

Dr. Chen Chu
Dr. Lantao Gou
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Genes is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • non-coding RNA
  • normal physiology
  • development
  • disease
  • biomarker
  • therapy

Published Papers (3 papers)

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Research

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23 pages, 2237 KiB  
Article
General Designs Reveal Distinct Codes in Protein-Coding and Non-Coding Human DNA
by Dana Cohen
Genes 2022, 13(11), 1970; https://doi.org/10.3390/genes13111970 - 28 Oct 2022
Cited by 1 | Viewed by 1114
Abstract
This study seeks to investigate distinct signatures and codes within different genomic sequence locations of the human genome. The promoter and other non-coding regions contain sites for the binding of biological particles, for processes such as transcription regulation. The specific rules and sequence [...] Read more.
This study seeks to investigate distinct signatures and codes within different genomic sequence locations of the human genome. The promoter and other non-coding regions contain sites for the binding of biological particles, for processes such as transcription regulation. The specific rules and sequence codes that govern this remain poorly understood. To derive these (codes), the general designs of sequence are investigated. Genomic signatures are a powerful tool for assessing the general designs of sequence, and cross-comparing different genomic regions for their distinct sequence properties. Through these genomic signatures, the relative non-random properties of sequences are also assessed. Furthermore, a binary components analysis is carried out making use of information theory ideas, to study the RY (purine/pyrimidine), WS (weak/strong) and KM (keto/amino) signatures in the sequences. From this comparison, it is possible to identify the relative importance of these properties within the various protein-coding and non-coding genomic locations. The results show that coding DNA has a strongly non-random WS signature, which reflects the genetic code, and the hydrogen-bond base pairing of codon–anti-codon interactions. In contrast, non-coding locations, such as the promoter, contain a distinct genomic signature. A prominent feature throughout non-coding DNA is a highly non-random RY signature, which is very different in nature to coding DNA, and suggests a structural-based RY code. This marks progress towards deciphering the unknown code(s) in non-protein-coding DNA, and a further understanding of the coding DNA. Additionally, it unravels how DNA carries information. These findings have implications for the most fundamental principles of biology, including knowledge of gene regulation, development and disease. Full article
(This article belongs to the Special Issue Small Non-coding RNAs in Normal Physiology, Development and Diseases)
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14 pages, 1457 KiB  
Article
MiR-18a-5p Targets Connective Tissue Growth Factor Expression and Inhibits Transforming Growth Factor β2-Induced Trabecular Meshwork Cell Contractility
by John Knox, George Bou-Gharios, Kevin J. Hamill and Colin E. Willoughby
Genes 2022, 13(8), 1500; https://doi.org/10.3390/genes13081500 - 22 Aug 2022
Cited by 5 | Viewed by 1960
Abstract
Increased trabecular meshwork (TM) cell and tissue contractility is a driver of the reduced outflow facility and elevation of intraocular pressure (IOP) associated with primary open-angle glaucoma (POAG). Connective tissue growth factor (CTGF) is an established mediator of TM cell contractility, and its [...] Read more.
Increased trabecular meshwork (TM) cell and tissue contractility is a driver of the reduced outflow facility and elevation of intraocular pressure (IOP) associated with primary open-angle glaucoma (POAG). Connective tissue growth factor (CTGF) is an established mediator of TM cell contractility, and its expression is increased in POAG due to transforming growth factor β 2 (TGFβ2) signalling. Inhibiting CTGF upregulation using microRNA (miRNA) mimetics could represent a new treatment option for POAG. A combination of in silico predictive tools and a literature review identified a panel of putative CTGF-targeting miRNAs. Treatment of primary human TM cells with 5 ng/mL TGFβ2 for 24 h identified miR-18a-5p as a consistent responder, being upregulated in cells from five different human donors. Transfection of primary donor TM cells with 20 nM synthetic miR-18a-5p mimic reduced TGFβ2-induced CTGF protein expression, and stable lentiviral-mediated overexpression of this miRNA reduced TGFβ2-induced contraction of collagen gels. Together, these findings identify miR-18a-5p as a mediator of the TGFβ2 response and a candidate therapeutic agent for glaucoma via its ability to inhibit CTGF-associated increased TM contractility. Full article
(This article belongs to the Special Issue Small Non-coding RNAs in Normal Physiology, Development and Diseases)
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18 pages, 12872 KiB  
Brief Report
Molecular Networks of Platinum Drugs and Their Interaction with microRNAs in Cancer
by Shihori Tanabe, Eger Boonstra, Taehun Hong, Sabina Quader, Ryuichi Ono, Horacio Cabral, Kazuhiko Aoyagi, Hiroshi Yokozaki, Edward J. Perkins and Hiroki Sasaki
Genes 2023, 14(11), 2073; https://doi.org/10.3390/genes14112073 - 13 Nov 2023
Viewed by 1230
Abstract
The precise mechanism of resistance to anti-cancer drugs such as platinum drugs is not fully revealed. To reveal the mechanism of drug resistance, the molecular networks of anti-cancer drugs such as cisplatin, carboplatin, oxaliplatin, and arsenic trioxide were analyzed in several types of [...] Read more.
The precise mechanism of resistance to anti-cancer drugs such as platinum drugs is not fully revealed. To reveal the mechanism of drug resistance, the molecular networks of anti-cancer drugs such as cisplatin, carboplatin, oxaliplatin, and arsenic trioxide were analyzed in several types of cancers. Since diffuse-type stomach adenocarcinoma, which has epithelial–mesenchymal transition (EMT)-like characteristics, is more malignant than intestinal-type stomach adenocarcinoma, the gene expression and molecular networks in diffuse- and intestinal-type stomach adenocarcinomas were analyzed. Analysis of carboplatin revealed the causal network in diffuse large B-cell lymphoma. The upstream regulators of the molecular networks of cisplatin-treated lung adenocarcinoma included the anti-cancer drug trichostatin A (TSA), a histone deacetylase inhibitor. The upstream regulator analysis of cisplatin revealed an increase in FAS, BTG2, SESN1, and CDKN1A, and the involvement of the tumor microenvironment pathway. The molecular networks were predicted to interact with several microRNAs, which may contribute to the identification of new drug targets for drug-resistant cancer. Analysis of oxaliplatin, a platinum drug, revealed that the SPINK1 pancreatic cancer pathway is inactivated in ischemic cardiomyopathy. The study showed the importance of the molecular networks of anti-cancer drugs and tumor microenvironment in the treatment of cancer resistant to anti-cancer drugs. Full article
(This article belongs to the Special Issue Small Non-coding RNAs in Normal Physiology, Development and Diseases)
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