Epigenetic Regulatory Networks in Cancer: Understanding the Mechanisms of Disease Progression

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 1106

Special Issue Editors


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Guest Editor
Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA
Interests: cancer; cell signaling; epigenetics; microRNA; targeted therapy; carcinogenesis; apoptosis
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Center for Cancer Researcg, National Cancer Institute, NIH, Bethesda, MD 20982, USA
Interests: cancer biology; stem cell research; iPSCs; epigenetics; immunotherapy; gene regulation; chromatin remodeling; drug discovery

Special Issue Information

Dear Colleagues,

Cancer remains a significant clinical challenge due to its aggressive nature, treatment resistance, and the complexity of its underlying mechanisms. Despite advancements in understanding cancer pathogenesis, many forms of cancer continue to have poor prognoses and limited therapeutic options. Recent studies have highlighted the critical role of epigenetic regulatory mechanisms in the development and progression of various cancers. This Special Issue aims to explore the intricate epigenetic landscape that governs cancer pathogenesis, focusing on key components such as DNA methylation, histone modifications, non-coding RNAs—including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs)—and chromatin remodeling. These factors play a crucial role in regulating gene expression and cellular behavior, contributing to the initiation and advancement of cancer.

This Special Issue will highlight recent advancements in epigenetic research, focusing on novel biomarkers for early detection and potential therapeutic targets that could lead to more effective and personalized treatment strategies. By integrating these insights, the research presented here holds the potential to improve patient outcomes and offer new avenues in the fight against cancer. Additionally, it will enhance the understanding of how epigenetic alterations impact cancer biology, potentially informing strategies against a wide range of malignancies. We welcome submissions ranging from basic research to translational studies, aiming to provide a comprehensive overview of the epigenetic regulatory networks involved in cancer.

Dr. Anand Singh
Dr. Sudheer Kumar Gara
Guest Editors

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Keywords

  • cancer
  • epigenetics
  • miRNAs
  • BAP1
  • DNMTs
  • tumor suppressor
  • oncogenes
  • histone modification
  • chromatin remodeling

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Published Papers (1 paper)

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Research

20 pages, 6384 KiB  
Article
Identification of Epigenetic Regulatory Networks of Gene Methylation–miRNA–Transcription Factor Feed-Forward Loops in Basal-like Breast Cancer
by Larissa M. Okano, Alexandre L. K. de Azevedo, Tamyres M. Carvalho, Jean Resende, Jessica M. Magno, Bonald C. Figueiredo, Tathiane M. Malta, Mauro A. A. Castro and Luciane R. Cavalli
Cells 2025, 14(16), 1235; https://doi.org/10.3390/cells14161235 - 10 Aug 2025
Viewed by 446
Abstract
Basal-like breast cancer (BLBC) is associated with poor prognosis, high recurrence rates, and limited therapeutic options, largely due to its molecular heterogeneity and complexity, which include epigenetic alterations. This study investigated epigenetic regulatory networks in BLBC by analyzing DNA methylation in distal cis-regulatory [...] Read more.
Basal-like breast cancer (BLBC) is associated with poor prognosis, high recurrence rates, and limited therapeutic options, largely due to its molecular heterogeneity and complexity, which include epigenetic alterations. This study investigated epigenetic regulatory networks in BLBC by analyzing DNA methylation in distal cis-regulatory regions and its impact on genes, transcription factors (TFs), and microRNAs (miRNAs) expression. Data from TCGA were processed using the ELMER and DESeq2 tools to identify differentially methylated regions and differentially expressed genes, TFs, and miRNAs. The FANMOD algorithm was used to identify the regulatory interactions uncovering the feed-forward loops (FFLs). The analysis identified 110 TF-mediated FFLs, 43 miRNA-mediated FFLs, and five composite FFLs, involving 18 hypermethylated and 32 hypomethylated genes, eight upregulated and nine downregulated TFs, and 21 upregulated and seven downregulated miRNAs. The TF-mediated FFLs major regulators involved the AR, EBF1, FOS, FOXM1, and TEAD4 TFs, while key miRNAs were miR-3662, miR-429, and miR-4434. Enriched pathways involved cAMP, ErbB, FoxO, p53, TGF-beta, Rap1, and Ras signaling. Differences in hallmark gene set categories reflected distinct methylation and miRNA expression profiles. Overall, this integrative analysis mapped the intricate epigenetic landscape of BLBC, emphasizing the role of FFLs as regulatory motifs that integrate DNA methylation, TFs, and miRNAs in orchestrating disease’s development and progression and offering potential targets for future diagnostic and therapeutic strategies. Full article
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