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Biomolecules
Special Issues
Epigenetic Drivers of Cancer Metastasis: From Methylation to Non-Coding RNAs
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Epigenetic Drivers of Cancer Metastasis: From Methylation to Non-Coding RNAs

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: 19 June 2026 | Viewed by 1607

Special Issue Editor

Dr. Toshifumi Hara

E-Mail Website
Guest Editor
Department of Biochemistry, School of Pharmacy, Aichi Gakuin University, Aichi, Japan
Interests: epigenetics; cancer metastasis; methylation; noncoding RNAs

Special Issue Information

Dear Colleagues,

This Special Issue aims to highlight how epigenetic mechanisms—including DNA and RNA methylation, as well as non-coding RNAs—drive cancer metastasis. Metastasis, the leading cause of cancer-related mortality, involves complex regulatory processes that are still not fully understood. Recent findings suggest that aberrant methylation of DNA and RNA has a significant impact on gene function and expression, thereby enhancing tumor invasiveness and metastatic potential. Additionally, non-coding RNAs, such as microRNAs and long non-coding RNAs, have emerged as modulators of metastasis through interactions with epigenetic modifiers.

We encourage researchers interested in recent epigenetic advances to contribute studies elucidating novel roles of epigenetic modifiers in cancer metastasis. Review articles covering related research are also welcome for consideration in this Special Issue.

Dr. Toshifumi Hara
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 250 words) can be sent to the Editorial Office for assessment.

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. Biomolecules 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 2700 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

  • epigenetics
  • metastasis
  • DNA methylation
  • RNA methylation
  • non-coding RNAs

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Published Papers (2 papers)

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Research

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23 pages, 1640 KB  
Article
miR-155-5p Silencing Does Not Alter BTLA Molecule Expression in CLL T Cells: Implications for Targeted Immunotherapy
by Agata Kosmaczewska, Lidia Ciszak, Anna Andrzejczak, Anna Tomkiewicz, Anna Partyka, Zofia Rojek-Gajda, Irena Frydecka, Dariusz Wołowiec, Tomasz Wróbel, Agnieszka Bojarska-Junak, Jacek Roliński and Lidia Karabon
Biomolecules 2025, 15(11), 1499; https://doi.org/10.3390/biom15111499 - 24 Oct 2025
Viewed by 501
Abstract
Given that we have demonstrated that miR-155-5p is increased in CLL PBMCs and that its reduction with inhibitory siRNA partially restores the immune checkpoint BTLA protein level in CLL B cells, risk stratification for using anti-miR-155-based immunotherapy in CLL seems reasonable, particularly with [...] Read more.
Given that we have demonstrated that miR-155-5p is increased in CLL PBMCs and that its reduction with inhibitory siRNA partially restores the immune checkpoint BTLA protein level in CLL B cells, risk stratification for using anti-miR-155-based immunotherapy in CLL seems reasonable, particularly with its potential impact on T cells. Therefore, we aimed to assess the role of miR-155-5p in the epigenetic modification of BTLA levels in CLL T cells, especially since we observed that BTLA expression unfavorably promotes increased proliferative activity and IL-4 secretion in T cells, thus suggesting BTLA malfunction in the CLL T cell subset. Transfection of PBMCs with an inhibitor of miR-155-5p (INH) led to about a ten-fold down-regulation of miR-155-5p levels compared to control siRNA (NC) both in CLL patients and healthy individuals (HC), as assessed by RT-qPCR. Additionally, we did not find any significant differences in BTLA protein expression in T cells after silencing miR-155-5p in either examined group. We demonstrated for the first time that immunotherapy approaches based on systemic administration of anti-miR-155-5p therapeutics would be a favorable strategy in CLL, since they do not affect BTLA expression in T cell populations and could benefit CLL patients with impaired BTLA levels on CLL cells. Full article
(This article belongs to the Special Issue Epigenetic Drivers of Cancer Metastasis: From Methylation to Non-Coding RNAs)
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Review

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27 pages, 1005 KB  
Review
Rewriting the Fate of Cancer: Epigenetic and Epitranscriptomic Regulators in the Metastatic Cascade
by Toshifumi Hara and Murugan Subramanian
Biomolecules 2025, 15(11), 1573; https://doi.org/10.3390/biom15111573 - 10 Nov 2025
Viewed by 873
Abstract
Metastasis is the leading cause of cancer-related mortality, representing a highly coordinated, multistep process in which malignant cells gain the ability to invade, survive in the circulation, and establish secondary tumors at distant sites. While genetic mutations initiate oncogenesis, accumulating evidence shows that [...] Read more.
Metastasis is the leading cause of cancer-related mortality, representing a highly coordinated, multistep process in which malignant cells gain the ability to invade, survive in the circulation, and establish secondary tumors at distant sites. While genetic mutations initiate oncogenesis, accumulating evidence shows that epigenetic and epitranscriptomic regulators, encompassing DNA methylation, RNA modifications, and noncoding RNAs (ncRNAs), reshape metastatic phenotypes. This review integrates current insights into these mechanisms and their crosstalk, with a primary focus on their methylation modification. Given their plasticity and potential reversibility, these regulators are attractive targets for therapeutic intervention. Defining the dynamic interplay between DNA and RNA modifications and ncRNAs provides a coherent framework for controlling metastasis and guides the development of precision epigenetic strategies and biomarkers. Future research that integrates multi-omics approaches and spatial transcriptomics will be essential for revealing the epigenetic and epitranscriptomic layers of the metastatic landscape. Full article
(This article belongs to the Special Issue Epigenetic Drivers of Cancer Metastasis: From Methylation to Non-Coding RNAs)
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