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MicroRNA (miRNA) Technology in Cancer

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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: 20 June 2026 | Viewed by 6528

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Dr. Duncan Ayers

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1. Directorate of Pharmacy, Mater Dei Hospital, Swatar MSD2090, Malta
2. Faculty of Biology, Medicine and Health, The University of Manchester, Oxford Road, Manchester M13 9PL, UK
Interests: non-coding RNA; genomic; microRNA; miRNA; oncology
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Dear Colleagues,

MicroRNA (miRNA) technology has emerged as a pivotal tool in cancer research, offering profound insights into tumor biology and therapeutic strategies. miRNAs are small, non-coding RNA molecules that regulate gene expression post-transcriptionally by binding to target messenger RNAs (mRNAs), leading to their degradation or translation inhibition. Aberrant miRNA expression is a hallmark of cancer, influencing critical processes such as cell proliferation, apoptosis, invasion, and metastasis.

In cancer, miRNAs can act as oncogenes (oncomiRs) or tumor suppressors, depending on their target genes. For instance, miR-21 is frequently upregulated in various cancers and promotes tumor progression by targeting tumor suppressor genes, whereas miR-34a, a tumor suppressor, is often downregulated. This dual role makes miRNAs attractive candidates for both biomarkers and therapeutic targets.

Advances in miRNA technology have facilitated the development of miRNA mimics and antagomirs (anti-miRNA oligonucleotides) for therapeutic purposes. miRNA-based diagnostics, using liquid biopsies, enable non-invasive cancer detection and monitoring. Furthermore, miRNA delivery systems, including nanoparticles and viral vectors, are being explored to enhance therapeutic precision and minimize off-target effects.

Despite challenges such as delivery efficiency and potential toxicity, miRNA technology holds immense promise in revolutionizing personalized cancer therapy and improving patient outcomes.

This Special Issue focuses on the trials and tribulations, together with successful breakthroughs concerning the implementation of miRNA technology for practical use in clinical oncology settings.

Dr. Duncan Ayers
Guest Editor

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Keywords

miRNA
microRNA
cancer
oncology
drug delivery
technology
non-coding RNA

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Published Papers (5 papers)

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Research

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28 pages, 5685 KB

Open AccessArticle

Let-7a and miR-34a Interplay Potent Suppressive Roles in Hepatocellular Carcinoma via Co-Targeting FNDC3B, IGF2 and SOX4

by Bangly Soliman, Ahmed Fawzy Ibrahim, Ahmed Salem, Mohamed Ghazy, Mahmoud T. Abo-Elfadl, Mahmoud ElHefnawi and Mario Flores

Int. J. Mol. Sci. 2026, 27(4), 1714; https://doi.org/10.3390/ijms27041714 - 10 Feb 2026

Viewed by 716

Abstract

Both let-7a and miR-34a have been repeatedly studied as pivotal suppressors for Hepatocellular carcinoma; however, their combined regulations remain to be fully elucidated. In the present study, we performed a comprehensive in silico analysis for let-7a and miR-34a using a wealth of updated tools: miRWalk, Genetrail and miRnet. In addition, our study is the first to quantify both miRs and their three predicted yet not experimentally validated oncogenic targets: FNDC3B, IGF2 and SOX4. This was assessed in HepG2 cell model following treatment by PEGP-vector expressing the miRs by MTT assay, florescence microscopy, qPCR and immune-florescence. Our bioinformatics analysis revealed a pool of common predicted hepatocarcinogenic targets shared by both let-7a and miR-34a. Importantly, three targets were identified as co-regulated through multiple canonical binding sites for each miR, and these had not been experimentally validated before. Furthermore, functional enrichment of these putative targets demonstrated their significant involvement in major and emerging HCC hallmarks, such as reprogramming of energy metabolism and evading immune destruction. These findings support our concept of simultaneous co-regulation of these oncogenes through the signaling networks and GO terms associated with both miRs. Consistently, our experimental results verified the significant overexpression of both miRs in HepG2 cells, leading to reduced tumor cell proliferation and decreased levels of the three oncogenic transcripts. Interestingly, miR-34a exhibited a superior suppression effect, reaching 38.7%, and SOX4 was identified as the most significantly downregulated target at both transcriptional and translational levels. Our findings provide new insights into the interconnected anti-HCC effects of let-7a and miR-34a and highlight the potential of applying their combined use to achieve the best therapeutic outcomes for this invasive tumor. Full article

(This article belongs to the Special Issue MicroRNA (miRNA) Technology in Cancer)

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13 pages, 2900 KB

Open AccessArticle

MicroRNA-1 Suppresses Tumor Progression and UHRF1 Expression in Cholangiocarcinoma

by Makoto Muto, Teruhide Ishigame, Takashi Kimura, Naoya Sato, Yasuhide Kofunato, Akira Kenjo, Hiroyuki Yamamoto, Yuhki Yokoyama, Hirofumi Yamamoto and Shigeru Marubashi

Int. J. Mol. Sci. 2025, 26(23), 11718; https://doi.org/10.3390/ijms262311718 - 3 Dec 2025

Viewed by 655

Abstract

MicroRNAs (miRNAs) have been shown to suppress tumor progression in several cancers, including cholangiocarcinoma; however, their mechanisms and roles remain largely unexplored. In this study, we aimed to identify novel miRNAs and molecules associated with cholangiocarcinoma progression. Using miRNA and mRNA microarrays from surgically resected specimens, we identified microRNA-1 (miR-1) as significantly downregulated in cholangiocarcinoma tissues and selected it for further analysis. In the in vitro assay, miR-1 was transfected into cholangiocarcinoma cell lines to assess its effect on tumor progression. Proliferation and migration/invasion assays demonstrated significant tumor suppression in miR-1-transfected cells. Additionally, cell cycle and apoptosis assays revealed an increase in cells in the G1 and G2/M phases, a decrease in the S phase, and an elevation in apoptosis rates in miR-1-transfected cells. Further analysis of the miRNA and mRNA microarray data identified ubiquitin-like with plant homeodomain and ring finger domains 1 (UHRF1) as a molecule potentially associated with miR-1. Quantitative RT-PCR and Western blotting analysis confirmed that UHRF1 expression was suppressed following miR-1 transfection. This study demonstrated that cholangiocarcinoma progression was suppressed by restoring miR-1 expression, suggesting that UHRF1 expression is involved in cholangiocarcinoma progression. The results of this study provide new insights into the molecular mechanisms underlying cholangiocarcinoma progression. Full article

(This article belongs to the Special Issue MicroRNA (miRNA) Technology in Cancer)

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16 pages, 3684 KB

Open AccessArticle

miR-7-5p and Importin-7 Regulate the p53 Dynamics and Stability in Malignant and Benign Thyroid Cells

by Abeer Al-Abdallah, Iman Jahanbani and Bashayer Al-Shammari

Int. J. Mol. Sci. 2025, 26(12), 5813; https://doi.org/10.3390/ijms26125813 - 17 Jun 2025

Cited by 1 | Viewed by 1524

Abstract

Thyroid carcinogenesis has multiple hallmarks, including evasion of tumor suppressors. Reactivation of wild-type p53 function is the ultimate goal in cancer therapy, which requires an understanding of the p53 suppression mechanism specific to the cancer type. MiR-7-5p and IPO7 are implicated in the pathogenesis of several human diseases. This work aims to investigate the role of miR-7-5p and IPO7 in p53 regulation in papillary thyroid cancer (PTC) cells. Primary cultured thyroid cells and FFPE thyroid tissues from PTC and benign cases were used. Functional experiments were performed by transfection with IPO7 siRNA or miR-7-5p mimic/inhibitor, followed by apoptosis and luciferase reporter assays, immunoblot assays, and RT-PCR. The expression and subcellular localization of IPO7, p53, MDM2, and ribosomal proteins (RPL11 and RPL5) were studied by immunofluorescence staining and confocal microscopy. The results show that IPO7 is overexpressed in PTC and regulated by miR-7-5p. Modulation of IPO7 expression in cultured thyroid cells altered the nucleocytoplasmic shuttling of p53, MDM2, RPL11, and RPL5, in addition to the p53 protein level and activity. The expression pattern of IPO7, p53, and MDM2 in cultured thyroid cells and clinical thyroid tissue specimens confirmed the association between IPO7 overexpression and reduced p53 stability in PTC. In conclusion, the data here show that p53 level and activity are differentially controlled in malignant and benign thyroid cells through miR-7-5P/IPO7-mediated regulation of RP-MDM2-p53 nucleocytoplasmic trafficking. In PTC, downregulation of miR-7-5p with consequent overexpression of IPO7 might be a protective mechanism used by cancer cells to evade p53 growth suppression during carcinogenesis. Full article

(This article belongs to the Special Issue MicroRNA (miRNA) Technology in Cancer)

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15 pages, 1163 KB

Open AccessArticle

The Potential and Limitations of the MinION/Yenos Platform for miRNA-Enabled Early Cancer Detection

by Aleena Rafiq and Anastassia Kanavarioti

Int. J. Mol. Sci. 2025, 26(8), 3822; https://doi.org/10.3390/ijms26083822 - 17 Apr 2025

Cited by 2 | Viewed by 2096

Abstract

The 2024 Nobel Prize in Physiology or Medicine was awarded to the pioneers who reported that microRNAs (miRNAs) regulate and direct the switch between physiological and pathological pathways via their over- or underexpression. The discovery changed the medical landscape and there are many completed and on-going clinical studies based on miRNAs. MiRNAs occur at the femtomolar level in biological fluids and are typically quantified using amplification-based techniques. Experimental nanopores have illustrated potential for trace analysis including amplification-free miRNA quantification. We repurposed the MinION, the only commercially available nanopore array device, and developed unique probes and protocols to detect and measure miRNA copies in blood and urine. Here, we report that miRNA copies are proportional to the total RNA isolated from the biospecimen, and that three known miRNA cancer biomarkers, i.e., miR-21, miR-375, and miR-141, were more than 1.5-fold overexpressed in blood samples from breast, ovarian, prostate, pancreatic, lung, and colorectal cancer patients compared to healthy patients. In these cancer samples, miR-15b was not overexpressed, in agreement with earlier studies. In contrast to literature reports, sample variability was undetectable in this study. The potential and limitations of this ready-to-use MinION/Yenos platform for multiple-cancer early detection (MCED) using blood or urine are discussed. Full article

(This article belongs to the Special Issue MicroRNA (miRNA) Technology in Cancer)

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Review

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28 pages, 1636 KB

Open AccessReview

Therapeutic microRNAs: Mechanisms, Delivery, and Clinical Translation in Oncology

by Humberto Vélez-Slimani and Luis A. Salazar

Int. J. Mol. Sci. 2026, 27(5), 2162; https://doi.org/10.3390/ijms27052162 - 25 Feb 2026

Viewed by 533

Abstract

MicroRNAs (miRNAs) are ~19–25-nt post-transcriptional regulators whose dysregulation promotes hallmark cancer traits and therapy resistance. This review synthesizes translational principles for developing miRNA therapeutics in oncology, integrating miRNA biology and target engagement with delivery design and clinical experience. We summarize key determinants that shape efficacy and safety, including sequence and chemistry choices, biodistribution and intracellular delivery, dosing strategy, and biomarker-informed patient selection. We compare the main therapeutic modalities, miRNA mimics and inhibitors, and evaluate leading delivery approaches relevant to cancer, including lipid-based systems, polymer-based carriers and conjugates, and extracellular vesicle-inspired platforms, highlighting trade-offs in stability, specificity, immune activation, and tumor exposure. Early clinical programs such as MRX34, TargomiR/MesomiR-1, and cobomarsen, together with experience from non-oncology indications, illustrate both opportunities and practical constraints on tolerability and regimen optimization. We conclude with pragmatic priorities for the field, including standardized analytics for isoforms and target engagement, PK/PD- and biomarker-guided dose selection, and rational combination strategies to safely integrate miRNA-based interventions into precision oncology. Full article

(This article belongs to the Special Issue MicroRNA (miRNA) Technology in Cancer)

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