Modulating epigenetic modifications for cancer therapy (Review)
Cancer is a global public health concern. Alterations in epigenetic processes are among the earliest genomic aberrations occurring during cancer development and are closely related to progression. Unlike genetic mutations, aberrations in epigenetic processes are reversible, which opens the possibili...
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Veröffentlicht in: | Oncology reports 2023-03, Vol.49 (3), p.1, Article 59 |
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description | Cancer is a global public health concern. Alterations in epigenetic processes are among the earliest genomic aberrations occurring during cancer development and are closely related to progression. Unlike genetic mutations, aberrations in epigenetic processes are reversible, which opens the possibility for novel pharmacological treatments. Non‑coding RNAs (ncRNAs) represent an essential epigenetic mechanism, and emerging evidence links ncRNAs to carcinogenesis. Epigenetic drugs (epidrugs) are a group of promising target therapies for cancer treatment acting as coadjuvants to reverse drug resistance in cancer. The present review describes central epigenetic aberrations during malignant transformation and explains how epidrugs target DNA methylation, histone modifications and ncRNAs. Furthermore, clinical trials focused on evaluating the effect of these epidrugs alone or in combination with other anticancer therapies and other ncRNA‑based therapies are discussed. The use of epidrugs promises to be an effective tool for reversing drug resistance in some patients with cancer. |
doi_str_mv | 10.3892/or.2023.8496 |
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Alterations in epigenetic processes are among the earliest genomic aberrations occurring during cancer development and are closely related to progression. Unlike genetic mutations, aberrations in epigenetic processes are reversible, which opens the possibility for novel pharmacological treatments. Non‑coding RNAs (ncRNAs) represent an essential epigenetic mechanism, and emerging evidence links ncRNAs to carcinogenesis. Epigenetic drugs (epidrugs) are a group of promising target therapies for cancer treatment acting as coadjuvants to reverse drug resistance in cancer. The present review describes central epigenetic aberrations during malignant transformation and explains how epidrugs target DNA methylation, histone modifications and ncRNAs. Furthermore, clinical trials focused on evaluating the effect of these epidrugs alone or in combination with other anticancer therapies and other ncRNA‑based therapies are discussed. The use of epidrugs promises to be an effective tool for reversing drug resistance in some patients with cancer.</description><identifier>ISSN: 1021-335X</identifier><identifier>ISSN: 1791-2431</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2023.8496</identifier><identifier>PMID: 36799181</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Antimitotic agents ; Antineoplastic agents ; Cancer ; Cancer therapies ; Carcinogenesis - genetics ; Care and treatment ; Cell division ; Chemical bonds ; Cyclin-dependent kinases ; Development and progression ; DNA ; DNA damage ; DNA Methylation ; Drug resistance ; Enzymes ; Epigenesis, Genetic ; Epigenetic inheritance ; Epigenetics ; FDA approval ; Gene expression ; Gene mutations ; Genetic aspects ; Genomes ; Health aspects ; Hematology ; Humans ; Kinases ; Methylation ; MicroRNAs ; Mutation ; Neoplasms - drug therapy ; Neoplasms - genetics ; Procainamide ; Review ; RNA ; RNA, Untranslated - metabolism ; X chromosomes</subject><ispartof>Oncology reports, 2023-03, Vol.49 (3), p.1, Article 59</ispartof><rights>COPYRIGHT 2023 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2023</rights><rights>Copyright: © Castro-Muñoz et al. 2023</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-b4b45ad133a92b84dcd92ab57185cbc6e47137166c725929773389b20e26cdd43</citedby><cites>FETCH-LOGICAL-c510t-b4b45ad133a92b84dcd92ab57185cbc6e47137166c725929773389b20e26cdd43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36799181$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Castro-Muñoz, Leonardo Josué</creatorcontrib><creatorcontrib>Ulloa, Elenaé Vázquez</creatorcontrib><creatorcontrib>Sahlgren, Cecilia</creatorcontrib><creatorcontrib>Lizano, Marcela</creatorcontrib><creatorcontrib>De La Cruz-Hernández, Erick</creatorcontrib><creatorcontrib>Contreras-Paredes, Adriana</creatorcontrib><title>Modulating epigenetic modifications for cancer therapy (Review)</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>Cancer is a global public health concern. Alterations in epigenetic processes are among the earliest genomic aberrations occurring during cancer development and are closely related to progression. Unlike genetic mutations, aberrations in epigenetic processes are reversible, which opens the possibility for novel pharmacological treatments. Non‑coding RNAs (ncRNAs) represent an essential epigenetic mechanism, and emerging evidence links ncRNAs to carcinogenesis. Epigenetic drugs (epidrugs) are a group of promising target therapies for cancer treatment acting as coadjuvants to reverse drug resistance in cancer. The present review describes central epigenetic aberrations during malignant transformation and explains how epidrugs target DNA methylation, histone modifications and ncRNAs. Furthermore, clinical trials focused on evaluating the effect of these epidrugs alone or in combination with other anticancer therapies and other ncRNA‑based therapies are discussed. The use of epidrugs promises to be an effective tool for reversing drug resistance in some patients with cancer.</description><subject>Antimitotic agents</subject><subject>Antineoplastic agents</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Carcinogenesis - genetics</subject><subject>Care and treatment</subject><subject>Cell division</subject><subject>Chemical bonds</subject><subject>Cyclin-dependent kinases</subject><subject>Development and progression</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA Methylation</subject><subject>Drug resistance</subject><subject>Enzymes</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetic inheritance</subject><subject>Epigenetics</subject><subject>FDA approval</subject><subject>Gene expression</subject><subject>Gene mutations</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Health aspects</subject><subject>Hematology</subject><subject>Humans</subject><subject>Kinases</subject><subject>Methylation</subject><subject>MicroRNAs</subject><subject>Mutation</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - genetics</subject><subject>Procainamide</subject><subject>Review</subject><subject>RNA</subject><subject>RNA, Untranslated - metabolism</subject><subject>X chromosomes</subject><issn>1021-335X</issn><issn>1791-2431</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkl1rFTEQhoMotlbvvJYFQSq4x3xuNjdKKVYLFUEUvAvZZPaclN3kNNmt9N-b7Zc9IrmYMHnmDTPzIvSS4BVrFX0f04piylYtV80jtE-kIjXljDwud0xJzZj4tYee5XyOMZW4UU_RHmukUqQl--jj1-jmwUw-rCvY-jUEmLytxuh8723Jx5CrPqbKmmAhVdMGktleVYff4dLD77fP0ZPeDBle3MYD9PPk04_jL_XZt8-nx0dntRUET3XHOy6MI4wZRbuWO-sUNZ2QpBW2sw1wSZgkTWMlFYoqKVlprqMYaGOd4-wAfbjR3c7dCM5CmJIZ9Db50aQrHY3Xuy_Bb_Q6XmqlOKWiKQKHtwIpXsyQJz36bGEYTIA4Z02lbBtMVCsL-vof9DzOKZT2CtVyyojg_C-1NgNoH_pY_rWLqD6SnFGmlFio1X-ochyM3sYAvS_5nYI3Dwo2YIZpk-MwX29iF3x3A9oUc07Q3w-DYL04Q8ekF2foxRkFf_VwgPfwnRXYH-xjsTE</recordid><startdate>20230301</startdate><enddate>20230301</enddate><creator>Castro-Muñoz, Leonardo Josué</creator><creator>Ulloa, Elenaé Vázquez</creator><creator>Sahlgren, Cecilia</creator><creator>Lizano, Marcela</creator><creator>De La Cruz-Hernández, Erick</creator><creator>Contreras-Paredes, Adriana</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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Alterations in epigenetic processes are among the earliest genomic aberrations occurring during cancer development and are closely related to progression. Unlike genetic mutations, aberrations in epigenetic processes are reversible, which opens the possibility for novel pharmacological treatments. Non‑coding RNAs (ncRNAs) represent an essential epigenetic mechanism, and emerging evidence links ncRNAs to carcinogenesis. Epigenetic drugs (epidrugs) are a group of promising target therapies for cancer treatment acting as coadjuvants to reverse drug resistance in cancer. The present review describes central epigenetic aberrations during malignant transformation and explains how epidrugs target DNA methylation, histone modifications and ncRNAs. Furthermore, clinical trials focused on evaluating the effect of these epidrugs alone or in combination with other anticancer therapies and other ncRNA‑based therapies are discussed. The use of epidrugs promises to be an effective tool for reversing drug resistance in some patients with cancer.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>36799181</pmid><doi>10.3892/or.2023.8496</doi><oa>free_for_read</oa></addata></record> |
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subjects | Antimitotic agents Antineoplastic agents Cancer Cancer therapies Carcinogenesis - genetics Care and treatment Cell division Chemical bonds Cyclin-dependent kinases Development and progression DNA DNA damage DNA Methylation Drug resistance Enzymes Epigenesis, Genetic Epigenetic inheritance Epigenetics FDA approval Gene expression Gene mutations Genetic aspects Genomes Health aspects Hematology Humans Kinases Methylation MicroRNAs Mutation Neoplasms - drug therapy Neoplasms - genetics Procainamide Review RNA RNA, Untranslated - metabolism X chromosomes |
title | Modulating epigenetic modifications for cancer therapy (Review) |
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