Histone Deacetylase Inhibitors Sensitize Murine B16F10 Melanoma Cells to Carbon Ion Irradiation by Inducing G1 Phase Arrest
Epigenetic processes, in addition to genetic abnormalities, play a critical role in refractory malignant diseases and cause the unresponsiveness to various chemotherapeutic regimens and radiotherapy. Herein we demonstrate that histone deacetylase inhibitors (HDACis) can be used to sensitize malignan...
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| Veröffentlicht in: | Biological & pharmaceutical bulletin 2017/06/01, Vol.40(6), pp.844-851 |
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| creator | Saito, Katsuyo Funayama, Tomoo Yokota, Yuichiro Murakami, Takashi Kobayashi, Yasuhiko |
| description | Epigenetic processes, in addition to genetic abnormalities, play a critical role in refractory malignant diseases and cause the unresponsiveness to various chemotherapeutic regimens and radiotherapy. Herein we demonstrate that histone deacetylase inhibitors (HDACis) can be used to sensitize malignant melanoma B16F10 cells to carbon ion irradiation. The cells were first treated with HDACis (romidepsin [FK228, depsipeptide], trichostatin A [TSA], valproic acid [VPA], and suberanilohydroxamic acid [SAHA, vorinostat]) and were then exposed to two types of radiation (carbon ions and gamma-rays). We found that HDACis enhanced the radiation-induced apoptosis and suppression of clonogenicity that was induced by irradiation, having a greater effect with carbon ion irradiation than with gamma-rays. Carbon ion irradiation and the HDACi treatment induced G2/M and G0/G1 cell cycle arrest, respectively. Thus, it is considered that HDACi treatment enhanced the killing effects of carbon ion irradiation against melanoma cells by inducing the arrest of G1 phase cells, which are sensitive to radiation due to a lack of DNA homologous recombination repair. Based on these findings, we propose that pretreatment with HDACis as radiosensitizers to induce G1 arrest combined with carbon ion irradiation may have clinical efficacy against refractory cancer. |
| doi_str_mv | 10.1248/bpb.b16-01025 |
| format | Article |
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Herein we demonstrate that histone deacetylase inhibitors (HDACis) can be used to sensitize malignant melanoma B16F10 cells to carbon ion irradiation. The cells were first treated with HDACis (romidepsin [FK228, depsipeptide], trichostatin A [TSA], valproic acid [VPA], and suberanilohydroxamic acid [SAHA, vorinostat]) and were then exposed to two types of radiation (carbon ions and gamma-rays). We found that HDACis enhanced the radiation-induced apoptosis and suppression of clonogenicity that was induced by irradiation, having a greater effect with carbon ion irradiation than with gamma-rays. Carbon ion irradiation and the HDACi treatment induced G2/M and G0/G1 cell cycle arrest, respectively. Thus, it is considered that HDACi treatment enhanced the killing effects of carbon ion irradiation against melanoma cells by inducing the arrest of G1 phase cells, which are sensitive to radiation due to a lack of DNA homologous recombination repair. Based on these findings, we propose that pretreatment with HDACis as radiosensitizers to induce G1 arrest combined with carbon ion irradiation may have clinical efficacy against refractory cancer.</description><identifier>ISSN: 0918-6158</identifier><identifier>EISSN: 1347-5215</identifier><identifier>DOI: 10.1248/bpb.b16-01025</identifier><identifier>PMID: 28566628</identifier><language>eng</language><publisher>Japan: The Pharmaceutical Society of Japan</publisher><subject>Animals ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - radiation effects ; Cancer ; Carbon ; carbon ion irradiation ; Cell cycle ; Cell Line, Tumor ; Chromatin ; combination therapy ; Diseases ; DNA repair ; Exposure ; G1 arrest ; G1 phase ; G1 Phase Cell Cycle Checkpoints - drug effects ; Gamma Rays ; Genetic abnormalities ; Heavy Ion Radiotherapy ; Histone deacetylase ; histone deacetylase inhibitor ; Histone Deacetylase Inhibitors - pharmacology ; Histones - metabolism ; Homologous recombination ; Homology ; Inhibitors ; Ion irradiation ; Ions ; Irradiation ; Melanoma ; Melanoma, Experimental - drug therapy ; Melanoma, Experimental - metabolism ; Melanoma, Experimental - radiotherapy ; Mice ; Radiation therapy ; Radiation-Sensitizing Agents - pharmacology ; radiosensitizer ; Radiosensitizers ; Skin cancer ; Trichostatin A ; Valproic acid</subject><ispartof>Biological and Pharmaceutical Bulletin, 2017/06/01, Vol.40(6), pp.844-851</ispartof><rights>2017 The Pharmaceutical Society of Japan</rights><rights>Copyright Japan Science and Technology Agency 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c746t-bdf44a3ee52a9138375e0e2b96d6564ea9938564d3714c9d32d13abfa3e8e9043</citedby><cites>FETCH-LOGICAL-c746t-bdf44a3ee52a9138375e0e2b96d6564ea9938564d3714c9d32d13abfa3e8e9043</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,1877,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28566628$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Saito, Katsuyo</creatorcontrib><creatorcontrib>Funayama, Tomoo</creatorcontrib><creatorcontrib>Yokota, Yuichiro</creatorcontrib><creatorcontrib>Murakami, Takashi</creatorcontrib><creatorcontrib>Kobayashi, Yasuhiko</creatorcontrib><creatorcontrib>Takasaki University of Health and Welfare</creatorcontrib><creatorcontrib>Gunma University</creatorcontrib><creatorcontrib>aDepartment of Quantum Biology</creatorcontrib><creatorcontrib>National Institutes for Quantum and Radiological Science and Technology (QST</creatorcontrib><creatorcontrib>cDepartment of Radiation-Applied Biology</creatorcontrib><creatorcontrib>Takasaki Advanced Radiation Research Institute (TARRI</creatorcontrib><creatorcontrib>Present address:Department of Microbiology</creatorcontrib><creatorcontrib>Graduate School of Medicine</creatorcontrib><creatorcontrib>Faculty of Pharmacy</creatorcontrib><creatorcontrib>Saitama Medical University</creatorcontrib><creatorcontrib>bLaboratory of Tumor Biology</creatorcontrib><creatorcontrib>Quantum Beam Science Research Directorate (QuBS</creatorcontrib><title>Histone Deacetylase Inhibitors Sensitize Murine B16F10 Melanoma Cells to Carbon Ion Irradiation by Inducing G1 Phase Arrest</title><title>Biological & pharmaceutical bulletin</title><addtitle>Biol Pharm Bull</addtitle><description>Epigenetic processes, in addition to genetic abnormalities, play a critical role in refractory malignant diseases and cause the unresponsiveness to various chemotherapeutic regimens and radiotherapy. Herein we demonstrate that histone deacetylase inhibitors (HDACis) can be used to sensitize malignant melanoma B16F10 cells to carbon ion irradiation. The cells were first treated with HDACis (romidepsin [FK228, depsipeptide], trichostatin A [TSA], valproic acid [VPA], and suberanilohydroxamic acid [SAHA, vorinostat]) and were then exposed to two types of radiation (carbon ions and gamma-rays). We found that HDACis enhanced the radiation-induced apoptosis and suppression of clonogenicity that was induced by irradiation, having a greater effect with carbon ion irradiation than with gamma-rays. Carbon ion irradiation and the HDACi treatment induced G2/M and G0/G1 cell cycle arrest, respectively. Thus, it is considered that HDACi treatment enhanced the killing effects of carbon ion irradiation against melanoma cells by inducing the arrest of G1 phase cells, which are sensitive to radiation due to a lack of DNA homologous recombination repair. Based on these findings, we propose that pretreatment with HDACis as radiosensitizers to induce G1 arrest combined with carbon ion irradiation may have clinical efficacy against refractory cancer.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - radiation effects</subject><subject>Cancer</subject><subject>Carbon</subject><subject>carbon ion irradiation</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Chromatin</subject><subject>combination therapy</subject><subject>Diseases</subject><subject>DNA repair</subject><subject>Exposure</subject><subject>G1 arrest</subject><subject>G1 phase</subject><subject>G1 Phase Cell Cycle Checkpoints - drug effects</subject><subject>Gamma Rays</subject><subject>Genetic abnormalities</subject><subject>Heavy Ion Radiotherapy</subject><subject>Histone deacetylase</subject><subject>histone deacetylase inhibitor</subject><subject>Histone Deacetylase Inhibitors - pharmacology</subject><subject>Histones - metabolism</subject><subject>Homologous recombination</subject><subject>Homology</subject><subject>Inhibitors</subject><subject>Ion irradiation</subject><subject>Ions</subject><subject>Irradiation</subject><subject>Melanoma</subject><subject>Melanoma, Experimental - drug therapy</subject><subject>Melanoma, Experimental - metabolism</subject><subject>Melanoma, Experimental - radiotherapy</subject><subject>Mice</subject><subject>Radiation therapy</subject><subject>Radiation-Sensitizing Agents - pharmacology</subject><subject>radiosensitizer</subject><subject>Radiosensitizers</subject><subject>Skin cancer</subject><subject>Trichostatin A</subject><subject>Valproic acid</subject><issn>0918-6158</issn><issn>1347-5215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1vEzEQxVcIRNPCkSuyxIXLFn-tvXssW5pGagUScLZs76RxtLGD7T0E_vl6mxIkDh5bmp_fG_tV1TuCLwnl7SezN5eGiBoTTJsX1YIwLuuGkuZltcAdaWtBmvasOk9pizGWmLLX1RltGyEEbRfVn1uXcvCArkFbyIdRJ0Arv3HG5RAT-g4-uex-A7qfoivcZyJuCEb3MGofdhr1MI4J5YB6HU3waDWvGPXgdHblbA5Fbpis8w9oSdC3zWxwFSOk_KZ6tdZjgrfP-0X18-bLj_62vvu6XPVXd7WVXOTaDGvONQNoqO4Ia5lsAAM1nRhEIzjormPlPXxgknDbDYwOhGmzLlda6DBnF9XHo-4-hl9TMVY7l2yZW3sIU1KkQG3XCUoK-uE_dBum6Mt0MyWIZFLMgvWRsjGkFGGt9tHtdDwogtWciiqpqJKKekql8O-fVSezg-FE_42hAMsjULrO6jH4sfz1P2-bpHFhDIpiIhXGHONZmyvc8rk0hLZSlHiLUn9U2qasH-BkpWN2doSnwThWYi6nAU9du9FRgWeP5gK1Cw</recordid><startdate>20170601</startdate><enddate>20170601</enddate><creator>Saito, Katsuyo</creator><creator>Funayama, Tomoo</creator><creator>Yokota, Yuichiro</creator><creator>Murakami, Takashi</creator><creator>Kobayashi, Yasuhiko</creator><general>The Pharmaceutical Society of Japan</general><general>Pharmaceutical Society of Japan</general><general>Japan Science and Technology Agency</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20170601</creationdate><title>Histone Deacetylase Inhibitors Sensitize Murine B16F10 Melanoma Cells to Carbon Ion Irradiation by Inducing G1 Phase Arrest</title><author>Saito, Katsuyo ; Funayama, Tomoo ; Yokota, Yuichiro ; Murakami, Takashi ; Kobayashi, Yasuhiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c746t-bdf44a3ee52a9138375e0e2b96d6564ea9938564d3714c9d32d13abfa3e8e9043</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - radiation effects</topic><topic>Cancer</topic><topic>Carbon</topic><topic>carbon ion irradiation</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Chromatin</topic><topic>combination therapy</topic><topic>Diseases</topic><topic>DNA repair</topic><topic>Exposure</topic><topic>G1 arrest</topic><topic>G1 phase</topic><topic>G1 Phase Cell Cycle Checkpoints - drug effects</topic><topic>Gamma Rays</topic><topic>Genetic abnormalities</topic><topic>Heavy Ion Radiotherapy</topic><topic>Histone deacetylase</topic><topic>histone deacetylase inhibitor</topic><topic>Histone Deacetylase Inhibitors - pharmacology</topic><topic>Histones - metabolism</topic><topic>Homologous recombination</topic><topic>Homology</topic><topic>Inhibitors</topic><topic>Ion irradiation</topic><topic>Ions</topic><topic>Irradiation</topic><topic>Melanoma</topic><topic>Melanoma, Experimental - drug therapy</topic><topic>Melanoma, Experimental - metabolism</topic><topic>Melanoma, Experimental - radiotherapy</topic><topic>Mice</topic><topic>Radiation therapy</topic><topic>Radiation-Sensitizing Agents - pharmacology</topic><topic>radiosensitizer</topic><topic>Radiosensitizers</topic><topic>Skin cancer</topic><topic>Trichostatin A</topic><topic>Valproic acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Saito, Katsuyo</creatorcontrib><creatorcontrib>Funayama, Tomoo</creatorcontrib><creatorcontrib>Yokota, Yuichiro</creatorcontrib><creatorcontrib>Murakami, Takashi</creatorcontrib><creatorcontrib>Kobayashi, Yasuhiko</creatorcontrib><creatorcontrib>Takasaki University of Health and Welfare</creatorcontrib><creatorcontrib>Gunma University</creatorcontrib><creatorcontrib>aDepartment of Quantum Biology</creatorcontrib><creatorcontrib>National Institutes for Quantum and Radiological Science and Technology (QST</creatorcontrib><creatorcontrib>cDepartment of Radiation-Applied Biology</creatorcontrib><creatorcontrib>Takasaki Advanced Radiation Research Institute (TARRI</creatorcontrib><creatorcontrib>Present address:Department of Microbiology</creatorcontrib><creatorcontrib>Graduate School of Medicine</creatorcontrib><creatorcontrib>Faculty of Pharmacy</creatorcontrib><creatorcontrib>Saitama Medical University</creatorcontrib><creatorcontrib>bLaboratory of Tumor Biology</creatorcontrib><creatorcontrib>Quantum Beam Science Research Directorate (QuBS</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Biological & pharmaceutical bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Saito, Katsuyo</au><au>Funayama, Tomoo</au><au>Yokota, Yuichiro</au><au>Murakami, Takashi</au><au>Kobayashi, Yasuhiko</au><aucorp>Takasaki University of Health and Welfare</aucorp><aucorp>Gunma University</aucorp><aucorp>aDepartment of Quantum Biology</aucorp><aucorp>National Institutes for Quantum and Radiological Science and Technology (QST</aucorp><aucorp>cDepartment of Radiation-Applied Biology</aucorp><aucorp>Takasaki Advanced Radiation Research Institute (TARRI</aucorp><aucorp>Present address:Department of Microbiology</aucorp><aucorp>Graduate School of Medicine</aucorp><aucorp>Faculty of Pharmacy</aucorp><aucorp>Saitama Medical University</aucorp><aucorp>bLaboratory of Tumor Biology</aucorp><aucorp>Quantum Beam Science Research Directorate (QuBS</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Histone Deacetylase Inhibitors Sensitize Murine B16F10 Melanoma Cells to Carbon Ion Irradiation by Inducing G1 Phase Arrest</atitle><jtitle>Biological & pharmaceutical bulletin</jtitle><addtitle>Biol Pharm Bull</addtitle><date>2017-06-01</date><risdate>2017</risdate><volume>40</volume><issue>6</issue><spage>844</spage><epage>851</epage><pages>844-851</pages><issn>0918-6158</issn><eissn>1347-5215</eissn><abstract>Epigenetic processes, in addition to genetic abnormalities, play a critical role in refractory malignant diseases and cause the unresponsiveness to various chemotherapeutic regimens and radiotherapy. Herein we demonstrate that histone deacetylase inhibitors (HDACis) can be used to sensitize malignant melanoma B16F10 cells to carbon ion irradiation. The cells were first treated with HDACis (romidepsin [FK228, depsipeptide], trichostatin A [TSA], valproic acid [VPA], and suberanilohydroxamic acid [SAHA, vorinostat]) and were then exposed to two types of radiation (carbon ions and gamma-rays). We found that HDACis enhanced the radiation-induced apoptosis and suppression of clonogenicity that was induced by irradiation, having a greater effect with carbon ion irradiation than with gamma-rays. Carbon ion irradiation and the HDACi treatment induced G2/M and G0/G1 cell cycle arrest, respectively. Thus, it is considered that HDACi treatment enhanced the killing effects of carbon ion irradiation against melanoma cells by inducing the arrest of G1 phase cells, which are sensitive to radiation due to a lack of DNA homologous recombination repair. Based on these findings, we propose that pretreatment with HDACis as radiosensitizers to induce G1 arrest combined with carbon ion irradiation may have clinical efficacy against refractory cancer.</abstract><cop>Japan</cop><pub>The Pharmaceutical Society of Japan</pub><pmid>28566628</pmid><doi>10.1248/bpb.b16-01025</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis Apoptosis - drug effects Apoptosis - radiation effects Cancer Carbon carbon ion irradiation Cell cycle Cell Line, Tumor Chromatin combination therapy Diseases DNA repair Exposure G1 arrest G1 phase G1 Phase Cell Cycle Checkpoints - drug effects Gamma Rays Genetic abnormalities Heavy Ion Radiotherapy Histone deacetylase histone deacetylase inhibitor Histone Deacetylase Inhibitors - pharmacology Histones - metabolism Homologous recombination Homology Inhibitors Ion irradiation Ions Irradiation Melanoma Melanoma, Experimental - drug therapy Melanoma, Experimental - metabolism Melanoma, Experimental - radiotherapy Mice Radiation therapy Radiation-Sensitizing Agents - pharmacology radiosensitizer Radiosensitizers Skin cancer Trichostatin A Valproic acid |
| title | Histone Deacetylase Inhibitors Sensitize Murine B16F10 Melanoma Cells to Carbon Ion Irradiation by Inducing G1 Phase Arrest |
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