Epigenetic changes are defined as inherited modifications that are not present in DNA sequence. Gene expression is regulated at various levels and not only in response to DNA modifications. Examples of epigenetic control are DNA methylation, histone deacetylation and mi-RNA expression. Methylation of several tumor suppressor gene promoters is responsible for their silencing and thus potentially sustain cancerogenesis. Similarly, histone deacetylation can lead to oncogene activation. mi-RNA are small (18–20 nucleotides) non-coding RNA fragments capable of inhibiting other m-RNA, ultimately altering the balance in oncogene and tumor suppressor gene expression. It has been shown that growth of several tumor types can be stimulated by epigenetic changes in various phases of cancerogenesis, and drugs able to interfere with these mechanisms can have a positive impact on tumor progression. As matter of fact, epigenetic changes are dynamic and can be reversed by epigenetic inhibitors. Recently, methyltransferase and histone deacetylase inhibitors have attracted the attention of researchers and clinicians as they potentially provide alternative therapeutic options in some cancers. Drugs that inhibit DNA methylation or histone deacetylation have been studied for the reactivation of tumor suppressor genes and repression of cancer cell growth. Epigenetic inhibitors work alone or in combination with other therapeutic agents. To date, a number of epigenetic inhibitors have been approved for cancer treatment. The main challenge in the field of epigenetic inhibitors is their lack of specificity. In this review article we describe their mechanisms of action and potential in cancer treatment.

Epigenetic control of gene expression: Potential implications for cancer treatment / Perri, F.; Longo, F.; Giuliano, M.; Sabbatino, F.; Favia, G.; Ionna, F.; Addeo, R.; Della Vittoria Scarpati, G.; Di Lorenzo, G.; Pisconti, S.. - In: CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY. - ISSN 1040-8428. - 111:(2017), pp. 166-172. [10.1016/j.critrevonc.2017.01.020]

Epigenetic control of gene expression: Potential implications for cancer treatment

Perri F.;Longo F.;Giuliano M.;Sabbatino F.;Addeo R.;Della Vittoria Scarpati G.;Di Lorenzo G.;
2017

Abstract

Epigenetic changes are defined as inherited modifications that are not present in DNA sequence. Gene expression is regulated at various levels and not only in response to DNA modifications. Examples of epigenetic control are DNA methylation, histone deacetylation and mi-RNA expression. Methylation of several tumor suppressor gene promoters is responsible for their silencing and thus potentially sustain cancerogenesis. Similarly, histone deacetylation can lead to oncogene activation. mi-RNA are small (18–20 nucleotides) non-coding RNA fragments capable of inhibiting other m-RNA, ultimately altering the balance in oncogene and tumor suppressor gene expression. It has been shown that growth of several tumor types can be stimulated by epigenetic changes in various phases of cancerogenesis, and drugs able to interfere with these mechanisms can have a positive impact on tumor progression. As matter of fact, epigenetic changes are dynamic and can be reversed by epigenetic inhibitors. Recently, methyltransferase and histone deacetylase inhibitors have attracted the attention of researchers and clinicians as they potentially provide alternative therapeutic options in some cancers. Drugs that inhibit DNA methylation or histone deacetylation have been studied for the reactivation of tumor suppressor genes and repression of cancer cell growth. Epigenetic inhibitors work alone or in combination with other therapeutic agents. To date, a number of epigenetic inhibitors have been approved for cancer treatment. The main challenge in the field of epigenetic inhibitors is their lack of specificity. In this review article we describe their mechanisms of action and potential in cancer treatment.
2017
Epigenetic control of gene expression: Potential implications for cancer treatment / Perri, F.; Longo, F.; Giuliano, M.; Sabbatino, F.; Favia, G.; Ionna, F.; Addeo, R.; Della Vittoria Scarpati, G.; Di Lorenzo, G.; Pisconti, S.. - In: CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY. - ISSN 1040-8428. - 111:(2017), pp. 166-172. [10.1016/j.critrevonc.2017.01.020]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/823822
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