MicroRNAs: Regulators of Cellular Fate

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 30 June 2026 | Viewed by 1897

Special Issue Editor

Special Issue Information

Dear Colleagues,

MicroRNAs (miRNAs) are among the most abundant non-coding RNAs and play a significant role in various biological processes, including disease progression. MicroRNAs are remarkably conserved across species, which reflects their essential biological functions. The evolutionary conservation of miRNAs strengthens their use as cross-species models for studying disease mechanisms and drug discovery. Understanding the gene regulation by miRNAs at the post-transcriptional level is therefore crucial. Indeed, the 2024 Nobel Prize in Physiology or Medicine was awarded to researchers for their discovery of miRNAs, thus highlighting the continuing importance of studying miRNAs.

In recent years, the identification of miRNA biomarkers for disease diagnosis has emerged as a prominent area of study. Beyond biomarker exploration, miRNA-based therapeutics—such as targeted treatments and drug discovery involving miRNAs—present exciting yet challenging opportunities for researchers. Utilizing miRNA biomarkers for diagnosis and miRNA-targeted treatments holds great promise for advancing personalized medicine. We therefore invite you to submit reviews and original research papers to this Special Issue on miRNA-related studies, including miRNA functionality through biological and computational approaches, the application of miRNA biomarkers, miRNA evolution, and other related topics.

Prof. Dr. Hsiuying Wang
Guest Editor

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Keywords

  • microRNA targets
  • microRNA conservation
  • microRNA pathway
  • microRNA mimics
  • microRNA antagonist
  • disease biomarker

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Published Papers (2 papers)

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Research

24 pages, 8383 KB  
Article
MicroRNA Deregulation and Immune Checkpoint Interactions in Common Variable Immunodeficiency and CLL-Associated Secondary Immunodeficiency
by Paulina Mertowska, Sebastian Mertowski, Milena Czosnek, Barbara Sosnowska-Pasiarska, Aleksandra Krasińska-Płachta, Zbigniew Krasiński, Tomasz Urbanowicz, Krzysztof Bojarski, Mansur Rahnama-Hezavah and Ewelina Grywalska
Cells 2025, 14(20), 1577; https://doi.org/10.3390/cells14201577 - 10 Oct 2025
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Abstract
Background: Immunodeficiencies are a heterogeneous group of disorders classified etiologically as primary (congenital) or secondary (acquired). Primary immunodeficiencies (PIDs), such as common variable immunodeficiency (CVID), result from genetic mutations that impair the development and function of lymphocytes. Secondary immunodeficiencies (SIDs) arise as a [...] Read more.
Background: Immunodeficiencies are a heterogeneous group of disorders classified etiologically as primary (congenital) or secondary (acquired). Primary immunodeficiencies (PIDs), such as common variable immunodeficiency (CVID), result from genetic mutations that impair the development and function of lymphocytes. Secondary immunodeficiencies (SIDs) arise as a consequence of chronic diseases, lymphoid malignancies, or immunosuppressive therapies. Aim of the study: The purpose of this study was to assess the serum expression profile of selected microRNAs (miRNAs) in patients with CVID and in those with chronic lymphocytic leukemia (CLL) and coexisting SID, compared to healthy individuals. Methods: Digital PCR (dPCR) was applied to quantify the serum expression levels of selected miRNAs in patients with CVID, patients with CLL and SID, and in healthy controls. Results: dPCR revealed significantly reduced levels of miR-16, miR-30c, miR-181a, miR-29a, miR-150, and miR-326 in the CVID group, potentially reflecting impaired regulatory mechanisms of the immune system. In contrast, elevated levels of miR-21, miR-125b, and miR-155 were observed in the CLL group with SID, suggesting their role in tumorigenesis and secondary immunosuppression. Correlations between miRNA levels and the expression of immune checkpoints (PD-1, CTLA-4, CD200) indicated the involvement of a complex regulatory network encompassing both humoral and cellular immune mechanisms. Conclusions: The results provide preliminary evidence that selected miRNAs could reflect disease-specific immune dysregulation patterns and may hold potential as diagnostic and prognostic biomarkers in both PIDs and SIDs. Full article
(This article belongs to the Special Issue MicroRNAs: Regulators of Cellular Fate)
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19 pages, 2817 KB  
Article
A Synthetic Sponge System Against miRNAs of the miR-17/92 Cluster Targets Transcriptional MYC Dosage Compensation in Aneuploid Cancer
by Diana M. Bravo-Estupiñan, Carsten Geiß, Jorge L. Arias-Arias, Mariela Montaño-Samaniego, Ricardo Chinchilla-Monge, Christian Marín-Müller, Steve Quirós-Barrantes, Anne Régnier-Vigouroux, Miguel Ibáñez-Hernández and Rodrigo A Mora-Rodríguez
Cells 2025, 14(17), 1384; https://doi.org/10.3390/cells14171384 - 4 Sep 2025
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Abstract
Background: Genomic instability, a hallmark of cancer, leads to copy number variations disrupting gene dosage balance and contributing to tumor progression. One of the most affected oncogenes is MYC, whose overexpression is tightly regulated to avoid cytotoxicity. In aneuploid cancer cells, gene dosage [...] Read more.
Background: Genomic instability, a hallmark of cancer, leads to copy number variations disrupting gene dosage balance and contributing to tumor progression. One of the most affected oncogenes is MYC, whose overexpression is tightly regulated to avoid cytotoxicity. In aneuploid cancer cells, gene dosage compensation mechanisms involving microRNAs (miRNAs) from the miR-17/92 cluster contribute in regulating MYC expression. Targeting this miRNA-mediated compensation system represents a promising therapeutic strategy leading to an uncontrolled and lethal MYC overexpression. Results: Synthetic miRNA sponges targeting miR-17, miR-19a, and miR-20a, key regulators of MYC dosage compensation, were designed and validated. Breast cancer cells (MCF7) with stable exogenous MYC overexpression were used to assess the impact of sponge constructs on MYC regulation. Quantitative RT-PCR revealed a significant reduction in miRNA expression and a corresponding increase in endogenous MYC levels upon sponge treatment. Functional assays in multiple colorectal cancer cell lines with varying MYC copy numbers demonstrated a time-dependent increase in cell death following sponge transfection. Cytotoxic effects increased with MYC copy number, confirming a correlation between gene dosage sensitivity and therapeutic response. Conclusions: Our findings demonstrate that miRNA sponges targeting the miR-17/92 cluster can effectively disrupt MYC dosage compensation, leading to selective cytotoxicity in MYC-amplified cancer cells. Full article
(This article belongs to the Special Issue MicroRNAs: Regulators of Cellular Fate)
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