Epigenetic and Epitranscriptomic Control in Prostate Cancer
Judith López1,2, Ana M Añazco-Guenkova1,2, Óscar Monteagudo-García1,2
1Centro de Investigación del Cáncer and Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-University of Salamanca, 37007 Salamanca, Spain.
Abstract:
The initiation of prostate cancer has been long associated with DNA copy-number alterations, the loss of specific chromosomal regions and gene fusions, and driver mutations, especially those of the Androgen Receptor. Non-mutational events, particularly DNA and RNA epigenetic dysregulation, are emerging as key players in tumorigenesis. In this review we summarize the molecular changes linked to epigenetic and epitranscriptomic dysregulation in prostate cancer and the role that alterations to DNA and RNA modifications play in the initiation and progression of prostate cancer.
Insights
Epigenetic and epitranscriptomic dysregulation, including DNA and RNA modifications, are key drivers in prostate cancer initiation and progression, alongside traditional genetic alterations. This review highlights these non-mutational events in prostate cancer development.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Prostate cancer initiation is linked to genetic changes like DNA copy-number alterations, chromosomal losses, gene fusions, and driver mutations (e.g., Androgen Receptor).
- Non-mutational events, specifically epigenetic and epitranscriptomic dysregulation, are increasingly recognized as critical factors in cancer development.
Purpose of the Study:
- To review the molecular changes associated with epigenetic and epitranscriptomic dysregulation in prostate cancer.
- To elucidate the role of DNA and RNA modifications in prostate cancer initiation and progression.
Main Methods:
- Literature review of studies on prostate cancer molecular alterations.
- Analysis of research focusing on epigenetic and epitranscriptomic changes.
- Synthesis of findings on DNA and RNA modifications in tumorigenesis.
Main Results:
- Epigenetic dysregulation (e.g., DNA methylation, histone modifications) impacts gene expression critical for prostate cancer.
- Epitranscriptomic alterations (e.g., RNA modifications like m6A) influence RNA stability, translation, and function, contributing to cancer.
- These non-mutational events interact with genetic factors to drive prostate cancer initiation and progression.
Conclusions:
- Epigenetic and epitranscriptomic alterations are fundamental to understanding prostate cancer development.
- Targeting these molecular changes offers potential new therapeutic strategies for prostate cancer.
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