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Updated: Jul 25, 2025
Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Cancer metastasis under the magnifying glass of epigenetics and epitranscriptomics
Maxime Janin1,2, Veronica Davalos1, Manel Esteller3,4,5,6
1Cancer Epigenetics Group, Josep Carreras Leukaemia Research Institute (IJC), IJC Building, Germans Trias I Pujol, Ctra de Can Ruti, Cami de Les Escoles S/N, 08916 Badalona, Barcelona, Spain.
Abstract:
Most of the cancer-associated mortality and morbidity can be attributed to metastasis. The role of epigenetic and epitranscriptomic alterations in cancer origin and progression has been extensively demonstrated during the last years. Both regulations share similar mechanisms driven by DNA or RNA modifiers, namely writers, readers, and erasers; enzymes responsible of respectively introducing, recognizing, or removing the epigenetic or epitranscriptomic modifications. Epigenetic regulation is achieved by DNA methylation, histone modifications, non-coding RNAs, chromatin accessibility, and enhancer reprogramming. In parallel, regulation at RNA level, named epitranscriptomic, is driven by a wide diversity of chemical modifications in mostly all RNA molecules. These two-layer regulatory mechanisms are finely controlled in normal tissue, and dysregulations are associated with every hallmark of human cancer. In this review, we provide an overview of the current state of knowledge regarding epigenetic and epitranscriptomic alterations governing tumor metastasis, and compare pathways regulated at DNA or RNA levels to shed light on a possible epi-crosstalk in cancer metastasis. A deeper understanding on these mechanisms could have important clinical implications for the prevention of advanced malignancies and the management of the disseminated diseases. Additionally, as these epi-alterations can potentially be reversed by small molecules or inhibitors against epi-modifiers, novel therapeutic alternatives could be envisioned.
Insights
Epigenetic and epitranscriptomic alterations drive cancer metastasis. Understanding these modifications and their crosstalk offers potential for new therapies against advanced cancers.
Area of Science:
- Molecular Biology
- Oncology
- Epigenetics
- Epitranscriptomics
Background:
- Cancer metastasis is a major cause of mortality and morbidity.
- Epigenetic and epitranscriptomic alterations are increasingly recognized in cancer development and progression.
- Both epigenetic and epitranscriptomic regulations involve enzymes (writers, readers, erasers) that modify DNA or RNA.
Purpose of the Study:
- To review current knowledge on epigenetic and epitranscriptomic alterations in tumor metastasis.
- To compare DNA- and RNA-level regulatory pathways involved in metastasis.
- To explore potential 'epi-crosstalk' mechanisms in cancer metastasis.
Main Methods:
- Literature review of epigenetic and epitranscriptomic mechanisms in cancer metastasis.
- Comparative analysis of DNA and RNA modification pathways.
- Discussion of potential clinical implications and therapeutic strategies.
Main Results:
- Dysregulation of epigenetic mechanisms (DNA methylation, histone modifications, etc.) and epitranscriptomic modifications (RNA chemical modifications) are linked to cancer hallmarks.
- These two regulatory layers share common modifier enzymes.
- A potential crosstalk between epigenetic and epitranscriptomic pathways in governing tumor metastasis is proposed.
Conclusions:
- Understanding epigenetic and epitranscriptomic alterations in metastasis is crucial for clinical applications.
- Targeting these 'epi-modifiers' could lead to novel therapeutic strategies for advanced malignancies.
- Further research into epi-crosstalk may reveal new avenues for preventing and managing disseminated cancer.
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