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Review

Epigenetic Modifications in Prostate Cancer

, , , , , , , , & show all
Pages 415-426 | Published online: 21 Oct 2014
 

Abstract

Prostate cancer is the most common cancer in men and the second leading cause of cancer deaths in men in France. Apart from the genetic alterations in prostate cancer, epigenetics modifications are involved in the development and progression of this disease. Epigenetic events are the main cause in gene regulation and the three most epigenetic mechanisms studied include DNA methylation, histone modifications and microRNA expression. In this review, we summarized epigenetic mechanisms in prostate cancer. Epigenetic drugs that inhibit DNA methylation, histone methylation and histone acetylation might be able to reactivate silenced gene expression in prostate cancer. However, further understanding of interactions of these enzymes and their effects on transcription regulation in prostate cancer is needed and has become a priority in biomedical research. In this study, we summed up epigenetic changes with emphasis on pharmacologic epigenetic target agents.

Financial & competing interests disclosure

The present paper was supported by grants from La Ligue contre le Cancer - Comites de la region Auvergne. S Karsli-Ceppioglu was supported by The Scientific and Technology Research Council of Turkey (TUBITAK-2219) project grants and A Dagdemir was supported by Protema Saglik Hizm. A.S. The authors declare that they have no competing interests. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

The present paper was supported by grants from La Ligue contre le Cancer - Comites de la region Auvergne. S Karsli-Ceppioglu was supported by The Scientific and Technology Research Council of Turkey (TUBITAK-2219) project grants and A Dagdemir was supported by Protema Saglik Hizm. A.S. The authors declare that they have no competing interests. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.

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