Epigenetic Mechanisms of Tumorigenesis

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

Deadline for manuscript submissions: 10 September 2025 | Viewed by 763

Special Issue Editor


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Guest Editor
Department of Internal Medicine, Division of Hematology, Oncology, and Palliative Care, Massey Cancer Institute, Virginia Commonwealth University, Richmond, VA 23298, USA
Interests: histone H2A deubiquitinase; tumorigenesis; ubiquitination; epigenetic mechanisms
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Special Issue Information

Dear Colleagues,

Tumorigenesis, the complex process by which normal cells transform into cancerous ones, is influenced by genetic mutations and epigenetic alterations. Epigenetic mechanisms, including DNA methylation, histone modifications, and non-coding RNA interactions, have a critical role in regulating gene expression without altering the underlying DNA sequence. These mechanisms are pivotal in maintaining cellular identity and function, but when disrupted, they can lead to aberrant gene expression profiles, contributing to cancer initiation and progression.

This Special Issue delves into the diverse epigenetic landscapes that drive tumorigenesis, exploring the latest research on how these modifications contribute to the onset and progression of various cancers. By understanding these processes, we can uncover novel biomarkers for early detection and therapeutic targets to develop more precise and effective cancer treatments. This compilation of studies and reviews provides a comprehensive overview of the current state of epigenetic research in oncology, highlighting both the challenges and opportunities in this rapidly evolving field.

Prof. Dr. Hengbin Wang
Guest Editor

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Keywords

  • epigenetics
  • tumorigenesis
  • gene expression
  • cell identity
  • precise medicine

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Published Papers (1 paper)

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Research

22 pages, 13702 KiB  
Article
MicroRNA miR-193b-3p Regulates Esophageal Cancer Progression Through Targeting RSF1
by Yao Lin, Xudong Zhao, Zhenhua Du, Zhili Jia, Siyu Zhou, Gengsheng Cao and Hengbin Wang
Cells 2025, 14(12), 928; https://doi.org/10.3390/cells14120928 - 19 Jun 2025
Viewed by 384
Abstract
Esophageal cancer (ESCA) is the sixth leading cause of cancer-related mortality worldwide. Despite the significant impact, the molecular mechanisms underlying its initiation and progression remain poorly understood. In this study, we identified mircoRNA miR-193b-3p as a critical regulator of ESCA progression and the [...] Read more.
Esophageal cancer (ESCA) is the sixth leading cause of cancer-related mortality worldwide. Despite the significant impact, the molecular mechanisms underlying its initiation and progression remain poorly understood. In this study, we identified mircoRNA miR-193b-3p as a critical regulator of ESCA progression and the Remodeling and Spacing Factor 1 (RSF1) as an essential target of miR-193b-3p. Analysis of the TCGA_ESCA dataset and RT-qPCR experiments revealed that RSF1 levels are significantly elevated in ESCA and inversely correlated with miR-193b-3p levels. Using a dual-luciferase reporter assay, as well as transfection of miR-193-3p mimics or inhibitors, we confirmed RSF1 as a direct target of miR-193b-3p in ESCA cells. Transfection of miR-193b-3p suppresses ESCA cell proliferation, migration, and invasion. These effects were partially reversed by exogenous RSF1 expression. Injection of AgomiR-193b-3p into mice bearing ESCA xenografts impeded tumor growth. These findings underscore the critical role of the miR-193b-3p/RSF1 axis in esophageal cancer progression. Full article
(This article belongs to the Special Issue Epigenetic Mechanisms of Tumorigenesis)
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