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The Roles of RNA (Coding and Non-coding) in Human Disease
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The Roles of RNA (Coding and Non-coding) in Human Disease

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

Deadline for manuscript submissions: 20 May 2025 | Viewed by 2176

Special Issue Editor

Dr. Lee Lee Wong

E-Mail Website
Guest Editor
1. Cardiovascular Research Institute, National University Health System, Singapore 117599, Singapore
2. Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117599, Singapore
Interests: biomarkers; microRNAs; therapeutic; cardiovascular disease; breast cancer; signalling

Special Issue Information

Dear Colleagues,

RNA plays a multifaceted role in human disease, influencing pathogenesis at various levels. Beyond its fundamental role in protein synthesis, RNA is being increasingly recognized for its regulatory functions, impacting gene expression and cellular processes. Coding RNA and non-coding RNA represent two broad categories of RNA molecules with distinct roles in cellular processes. Coding RNA directs protein synthesis, and disruptions in its functionality contribute to diseases like cancer and neurodegeneration. Non-coding RNA, including microRNAs and long non-coding RNAs, intricately modulate gene expression and are implicated in diverse pathologies. RNA’s utility as a biomarker for disease diagnosis and prognosis is expanding, given its differential expression profiles in various conditions. Moreover, understanding RNA’s functional nuances provides insights into disease mechanisms, offering potential therapeutic targets. Innovative RNA-based therapies, such as RNA interference and antisense oligonucleotides, hold promise for precision medicine by targeting specific disease-related RNA aberrations. Unraveling the complex interplay of coding and non-coding RNA in human diseases not only refines diagnostic approaches but also opens avenues for developing novel, targeted therapeutics. In this Special Issue, we welcome the submission of research articles and full reviews.

Dr. Lee Lee Wong
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • coding RNA
  • non-coding RNA
  • biomarker
  • functional role
  • therapeutic targets
 

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Published Papers (2 papers)

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Research

16 pages, 7146 KiB  
Article
MicroRNA Inhibiting Atheroprotective Proteins in Patients with Unstable Angina Comparing to Chronic Coronary Syndrome
by Michał Kowara, Michał Kopka, Karolina Kopka, Renata Głowczyńska, Karolina Mitrzak, Dan-ae Kim, Karol Artur Sadowski and Agnieszka Cudnoch-Jędrzejewska
Int. J. Mol. Sci. 2024, 25(19), 10621; https://doi.org/10.3390/ijms251910621 - 2 Oct 2024
Viewed by 633
Abstract
Patients with unstable angina present clinical characteristics of atherosclerotic plaque vulnerability, contrary to chronic coronary syndrome patients. The process of athersclerotic plaque destabilization is also regulated by microRNA particles. In this study, the investigation on expression levels of microRNAs inhibiting the expression of [...] Read more.
Patients with unstable angina present clinical characteristics of atherosclerotic plaque vulnerability, contrary to chronic coronary syndrome patients. The process of athersclerotic plaque destabilization is also regulated by microRNA particles. In this study, the investigation on expression levels of microRNAs inhibiting the expression of proteins that protect from atherosclerotic plaque progression (miR-92a inhibiting KLF2, miR-10b inhibiting KLF4, miR-126 inhibiting MerTK, miR-98 inhibiting IL-10, miR-29b inhibiting TGFβ1) was undertaken. A number of 62 individuals were enrolled—unstable angina (UA, n = 14), chronic coronary syndrome (CCS, n = 38), and healthy volunteers (HV, n = 10). Plasma samples were taken, and microRNAs expression levels were assessed by qRT-PCR. As a result, the UA patients presented significantly increased miR-10b levels compared to CCS patients (0.097 vs. 0.058, p = 0.033). Moreover, in additional analysis when UA patients were grouped together with stable patients with significant plaque in left main or proximal left anterior descending (“UA and LM/proxLAD” group, n = 29 patients) and compared to CCS patients with atherosclerotic lesions in other regions of coronary circulation (“CCS other” group, n = 25 patients) the expression levels of both miR-10b (0.104 vs. 0.046; p = 0.0032) and miR-92a (92.64 vs. 54.74; p = 0.0129) were significantly elevated. In conclusion, the study revealed significantly increased expression levels of miR-10b and miR-92a, a regulator of endothelial protective KLF factors (KLF4 and KLF2, respectively) in patients with more vulnerable plaque phenotypes. Full article
(This article belongs to the Special Issue The Roles of RNA (Coding and Non-coding) in Human Disease)
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19 pages, 7067 KiB  
Article
MEG3-Mediated Oral Squamous-Cell-Carcinoma-Derived Exosomal miR-421 Activates Angiogenesis by Targeting HS2ST1 in Vascular Endothelial Cells
by Chia-Yun Huang, Sung-Tau Chou, Yuan-Ming Hsu, Wan-Ju Chao, Guan-Hsun Wu, Jenn-Ren Hsiao, Horng-Dar Wang and Shine-Gwo Shiah
Int. J. Mol. Sci. 2024, 25(14), 7576; https://doi.org/10.3390/ijms25147576 - 10 Jul 2024
Viewed by 1080
Abstract
Exosomal microRNAs (miRNAs) from cancer cells play a key role in mediating the oral squamous cell carcinoma (OSCC) microenvironment. The objective of this study was to investigate how the long non-coding RNA (lncRNA) MEG3 affects OSCC angiogenesis through exosomal miR-421. Global miRNA microarray [...] Read more.
Exosomal microRNAs (miRNAs) from cancer cells play a key role in mediating the oral squamous cell carcinoma (OSCC) microenvironment. The objective of this study was to investigate how the long non-coding RNA (lncRNA) MEG3 affects OSCC angiogenesis through exosomal miR-421. Global miRNA microarray analysis and quantitative real-time PCR (qRT-PCR) were performed to determine the level of miRNAs in OSCC cell-derived exosomes. Cell migration, invasion, tube formation, immunohistochemistry, and hemoglobin concentrations were used to study the effects of exosomal miR-421 in angiogenesis. Western blotting was used to determine the expression level of HS2ST1 and VEGFR2-related downstream proteins. MiRNA array and qRT-PCR identified the upregulation of miR-421 in OSCC cell-derived exosomes. Furthermore, exosomal miR-421 can be taken up by human umbilical vein endothelial cells (HUVECs) and then target HS2ST1 through VEGF-mediated ERK and AKT phosphorylation, thereby promoting HUVEC migration, invasion, and tube formation. Additionally, forced expression of the lncRNA MEG3 in OSCC cells reduced exosomal miR-421 levels and then increased HS2ST1 expression, thereby reducing the VEGF/VEGFR2 pathway in HUVECs. Our results demonstrate a novel mechanism by which lncRNA MEG3 can act as a tumor suppressor and regulate endothelial angiogenesis through the exosomal miR-421/HS2ST1 axis, which provides a potential therapeutic strategy for OSCC angiogenesis. Full article
(This article belongs to the Special Issue The Roles of RNA (Coding and Non-coding) in Human Disease)
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