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Updated: May 6, 2026
Methylated DNA Immunoprecipitation
Published on: January 2, 2009
Cancer development, progression, and therapy: an epigenetic overview
Sibaji Sarkar1, Garrick Horn, Kimberly Moulton
1Cancer Center, L913, Department of Medicine, Boston University School of Medicine, 72 East Concord Street, Boston, MA 02118, USA. ss1@bu.edu.
Abstract:
Carcinogenesis involves uncontrolled cell growth, which follows the activation of oncogenes and/or the deactivation of tumor suppression genes. Metastasis requires down-regulation of cell adhesion receptors necessary for tissue-specific, cell-cell attachment, as well as up-regulation of receptors that enhance cell motility. Epigenetic changes, including histone modifications, DNA methylation, and DNA hydroxymethylation, can modify these characteristics. Targets for these epigenetic changes include signaling pathways that regulate apoptosis and autophagy, as well as microRNA. We propose that predisposed normal cells convert to cancer progenitor cells that, after growing, undergo an epithelial-mesenchymal transition. This process, which is partially under epigenetic control, can create a metastatic form of both progenitor and full-fledged cancer cells, after which metastasis to a distant location may occur. Identification of epigenetic regulatory mechanisms has provided potential therapeutic avenues. In particular, epigenetic drugs appear to potentiate the action of traditional therapeutics, often by demethylating and re-expressing tumor suppressor genes to inhibit tumorigenesis. Epigenetic drugs may inhibit both the formation and growth of cancer progenitor cells, thus reducing the recurrence of cancer. Adopting epigenetic alteration as a new hallmark of cancer is a logical and necessary step that will further encourage the development of novel epigenetic biomarkers and therapeutics.
Insights
Epigenetic alterations drive cancer development and metastasis by altering cell growth and adhesion. Epigenetic drugs offer new therapeutic strategies by targeting these changes, potentially inhibiting cancer recurrence.
Area of Science:
- Oncology
- Epigenetics
- Molecular Biology
Background:
- Carcinogenesis involves oncogene activation and tumor suppressor gene deactivation, leading to uncontrolled cell growth.
- Metastasis requires changes in cell adhesion and motility, often involving receptor regulation.
- Epigenetic modifications like DNA methylation and histone changes influence cancer progression.
Purpose of the Study:
- To explore the role of epigenetic alterations in cancer development, from progenitor cells to metastasis.
- To investigate how epigenetic changes affect key cellular processes like cell adhesion, motility, apoptosis, and autophagy.
- To highlight the therapeutic potential of targeting epigenetic mechanisms in cancer treatment.
Main Methods:
- The study proposes a model of cancer development involving epigenetic control of cell transformation and epithelial-mesenchymal transition.
- It reviews the impact of epigenetic modifications on signaling pathways and microRNAs.
- It discusses the therapeutic strategies involving epigenetic drugs and their mechanisms of action.
Main Results:
- Epigenetic changes are proposed to drive the conversion of normal cells to cancer progenitor cells and facilitate metastasis.
- Epigenetic modifications influence pathways regulating apoptosis, autophagy, and microRNA expression.
- Epigenetic drugs can re-express tumor suppressor genes, inhibit cancer growth, and reduce recurrence.
Conclusions:
- Epigenetic alterations are crucial in cancer initiation, progression, and metastasis.
- Targeting epigenetic mechanisms with drugs offers a promising therapeutic approach, potentially enhancing traditional treatments.
- Recognizing epigenetic alteration as a hallmark of cancer will spur the development of new biomarkers and therapies.
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