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Epigenetics and Chromatin Remodeling in Cancer

A Special Issue of Current Issues in Molecular Biology (ISSN 1467-3045) belonging to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 2049

Editors


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Guest Editor
AUSL Romagna—Centro Servizi Pievesestina, 47522 Cesena, Italy
Interests: hereditary cancer; next-generation sequencing; cancer genetics; cancer epigenetics; molecular characterization
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Biosciences Laboratory, IRCCS Istituto Romagnolo per lo Studio dei Tumori (IRST) “Dino Amadori”, 47014 Meldola, Italy
Interests: liquid biopsy; circulating tumor DNA; next-generation sequencing; precision oncology; cancer genomics; breast and urogenital cancer; molecular biomarkers; treatment resistance

Special Issue Information

Dear Colleagues,

Epigenetic modifications and chromatin remodeling play central roles in cancer by dynamically regulating gene expression without altering DNA sequences. Aberrant DNA methylation, histone modifications, and chromatin accessibility changes, often driven by somatic variants in non-coding or regulatory regions, can activate oncogenes or silence tumor suppressors, contributing to tumor initiation and progression.

This Special Issue explores recent advances in understanding the molecular mechanisms underlying epigenetic dysregulation and chromatin remodeling in cancer. We highlight novel technologies such as Methyl-seq, ATAC-seq, ChIP-seq, single-cell epigenomics, RNA-seq, and liquid biopsy approaches for detecting epigenetic alterations in circulating tumor DNA (ctDNA), which offer promising non-invasive cancer biomarkers and variant validation strategies.

We also discuss how DNA methylation, key chromatin remodelers, histone-modifying enzymes, and non-coding RNAs influence the epigenome in cancer.

The Special Issue also covers emerging therapeutic strategies, including epigenetic inhibitors and targeted chromatin-modifying drugs. By integrating findings from epigenetics, functional genomics, and precision oncology, this collection aims to provide a comprehensive perspective on chromatin dynamics in cancer and the potential for clinical applications.

Dr. Gianluca Tedaldi
Dr. Alessandra Virga
Guest Editors

Manuscript Submission Information

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Keywords

  • epigenetics
  • chromatin remodeling
  • DNA methylation
  • histone modifications
  • non-coding RNAs
  • circulating tumor DNA
  • liquid biopsy
  • epigenetic therapy

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Published Papers (2 papers)

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Review

17 pages, 1339 KB  
Review
SnoRNA and SNHG in Bladder Cancer: Molecular Mechanisms and Clinical Significance
by Galiya Gimalova, Irina Gilyazova, Elza Khusnutdinova and Valentin Pavlov
Curr. Issues Mol. Biol. 2026, 48(7), 662; https://doi.org/10.3390/cimb48070662 - 27 Jun 2026
Viewed by 521
Abstract
This review summarizes current data on the role of small nucleolar RNAs (snoRNAs) and their host genes (SNHGs) in the development of bladder cancer (BC). It examines snoRNA biogenesis, classical functions (rRNA modification), and non-canonical oncogenic mechanisms, including microRNA sponging, sdRNA [...] Read more.
This review summarizes current data on the role of small nucleolar RNAs (snoRNAs) and their host genes (SNHGs) in the development of bladder cancer (BC). It examines snoRNA biogenesis, classical functions (rRNA modification), and non-canonical oncogenic mechanisms, including microRNA sponging, sdRNA production, and protein interactions (EZH2, DNMT3A, hnRNPK). The factors involved in the deregulation of snoRNA/SNHG expression during tumour transformation are described, such as amplifications, epigenetic changes, and transcriptional control (c-Myc, p53). Studies have shown that in BC, the majority of snoRNAs/SNHGs (SNHG1, SNHG3, SNHG6, SNHG13, SCARNA12) act as oncogenes, activating the PI3K/AKT, Wnt/β-catenin, NF-κB, and c-Myc pathways, thereby enhancing proliferation, EMT, invasion, and metastasis. Suppressor molecules (SNHG2/GAS5) are also discussed. The clinical potential of snoRNAs as prognostic signatures (SNORS), diagnostic biomarkers (SNHG1 in urine), and therapeutic targets (e.g., SNHG3) is analyzed. Thus, snoRNAs and SNHGs represent a promising class of molecules for the development of new diagnostic and therapeutic approaches for BC, although further investigation in prospective studies is required. Full article
(This article belongs to the Special Issue Epigenetics and Chromatin Remodeling in Cancer)
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29 pages, 6102 KB  
Review
Metabolic Signaling Meets Epigenetic Regulation: How Protein Lactylation Remodels the Tumor Immune Microenvironment in Gastric Cancer
by Xiaoxuan Pan, Xin Chen, Chunyuan Zhang, Xin Ma and Jieru Han
Curr. Issues Mol. Biol. 2026, 48(6), 595; https://doi.org/10.3390/cimb48060595 - 4 Jun 2026
Viewed by 896
Abstract
This review argues that protein lactylation—a lactate-driven posttranslational modification—serves as the long-sought molecular bridge that coordinates these two hallmarks in gastric cancer (GC). Far from being a passive metabolic byproduct, lactylation operates as a central molecular hub with a dual function: intracellularly, it [...] Read more.
This review argues that protein lactylation—a lactate-driven posttranslational modification—serves as the long-sought molecular bridge that coordinates these two hallmarks in gastric cancer (GC). Far from being a passive metabolic byproduct, lactylation operates as a central molecular hub with a dual function: intracellularly, it directly drives malignant phenotypes by modifying key oncoproteins such as YAP and metabolic enzymes; extracellularly, it remodels the tumor immune microenvironment by polarizing tumor-associated macrophages toward an immunosuppressive M2 phenotype, upregulating PD-L1 expression, and impairing CD8+ T-cell function. We propose that these two arms constitute a self-reinforcing metabolic–epigenetic–immunological circuit, wherein lactylation both originates from and perpetuates the Warburg effect, creating a vicious cycle that sustains malignancy and immune evasion. This framework positions lactylation not merely as a mechanistic detail, but as a unifying principle that integrates metabolic reprogramming, epigenetic regulation, and immune suppression in GC. We critically evaluate the current landscape of lactylation “writers,” “erasers,” and “readers”; highlight the translational potential of targeting this pathway; and identify the conceptual and technical bottlenecks that must be overcome—including the lack of causality in current studies, the absence of specific research tools, and the unresolved heterogeneity of lactylation across cell types and disease stages. By reframing lactylation as an actionable hub rather than a downstream consequence, this review provides a roadmap for advancing lactylation-based precision medicine in GC. Full article
(This article belongs to the Special Issue Epigenetics and Chromatin Remodeling in Cancer)
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