The BRCA2 gene is a potential molecular target during 5-fluorouracil therapy in human oral cancer cells
5-Fluorouracil (5-FU) is widely used in clinical cancer therapy. It is commonly used either alone or in combination with other drugs and/or radiation for head and neck, and other types of cancers. 5-FU induces DNA double-strand breaks (DSBs). Inhibition of the repair of 5-FU-induced DSBs may improve...
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| Veröffentlicht in: | Oncology reports 2014-05, Vol.31 (5), p.2001-2006 |
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| creator | NAKAGAWA, YOSUKE KAJIHARA, ATSUHISA TAKAHASHI, AKIHISA KONDO, NATSUKO MORI, EIICHIRO KIRITA, TADAAKI OHNISHI, TAKEO |
| description | 5-Fluorouracil (5-FU) is widely used in clinical cancer therapy. It is commonly used either alone or in combination with other drugs and/or radiation for head and neck, and other types of cancers. 5-FU induces DNA double-strand breaks (DSBs). Inhibition of the repair of 5-FU-induced DSBs may improve the therapeutic response in many tumors to this anticancer agent. The aim of the present study was to further our understanding of the pathways which are involved in the repair of 5-FU-induced DSBs. Cell survival after drug treatment was examined with colony forming assays using Chinese hamster lung fibroblast cells or Chinese hamster ovary cell lines which are deficient in DSB repair pathways involving the homologous recombination repair-related genes BRCA2 and XRCC2, and the non-homologous end joining repair-related genes DNA-PKcs and Ku80. It was found that BRCA2 was involved in such repair, and may be effectively targeted to inhibit the repair of 5-FU-induced damage. Observations showed that knockdown of BRCA2 using small interference RNA suppression increased the sensitivity to 5-FU of human oral cancer cell lines (SAS and HSC3). These findings suggest that downregulation of BRCA2 may be useful for sensitizing tumor cells during 5-FU chemotherapy. |
| doi_str_mv | 10.3892/or.2014.3080 |
| format | Article |
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It is commonly used either alone or in combination with other drugs and/or radiation for head and neck, and other types of cancers. 5-FU induces DNA double-strand breaks (DSBs). Inhibition of the repair of 5-FU-induced DSBs may improve the therapeutic response in many tumors to this anticancer agent. The aim of the present study was to further our understanding of the pathways which are involved in the repair of 5-FU-induced DSBs. Cell survival after drug treatment was examined with colony forming assays using Chinese hamster lung fibroblast cells or Chinese hamster ovary cell lines which are deficient in DSB repair pathways involving the homologous recombination repair-related genes BRCA2 and XRCC2, and the non-homologous end joining repair-related genes DNA-PKcs and Ku80. It was found that BRCA2 was involved in such repair, and may be effectively targeted to inhibit the repair of 5-FU-induced damage. Observations showed that knockdown of BRCA2 using small interference RNA suppression increased the sensitivity to 5-FU of human oral cancer cell lines (SAS and HSC3). These findings suggest that downregulation of BRCA2 may be useful for sensitizing tumor cells during 5-FU chemotherapy.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2014.3080</identifier><identifier>PMID: 24627042</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>5-fluorouracil ; Animals ; Antimetabolites, Antineoplastic - pharmacology ; BRCA2 ; BRCA2 Protein - genetics ; Cancer therapies ; Cell cycle ; Cell Line, Tumor ; Cell Survival - drug effects ; Chemotherapy ; CHO Cells ; Cricetinae ; Cricetulus ; Deoxyribonucleic acid ; DNA ; DNA Breaks, Double-Stranded - drug effects ; DNA repair ; DNA Repair - drug effects ; double-strand breaks ; Enzymes ; Fibroblasts ; Flow cytometry ; Fluorouracil - pharmacology ; Humans ; M Phase Cell Cycle Checkpoints - drug effects ; Metabolism ; Metabolites ; Mice ; Mouth Neoplasms - drug therapy ; Mouth Neoplasms - genetics ; Oral cancer ; oral cancer cells ; Proteins ; RNA Interference ; RNA, Small Interfering ; Rodents</subject><ispartof>Oncology reports, 2014-05, Vol.31 (5), p.2001-2006</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c454t-37054f3abe88511253f7e2fdf93b8429b3a1eb66fe6cd5c057abf4cb861327013</citedby><cites>FETCH-LOGICAL-c454t-37054f3abe88511253f7e2fdf93b8429b3a1eb66fe6cd5c057abf4cb861327013</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24627042$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>NAKAGAWA, YOSUKE</creatorcontrib><creatorcontrib>KAJIHARA, ATSUHISA</creatorcontrib><creatorcontrib>TAKAHASHI, AKIHISA</creatorcontrib><creatorcontrib>KONDO, NATSUKO</creatorcontrib><creatorcontrib>MORI, EIICHIRO</creatorcontrib><creatorcontrib>KIRITA, TADAAKI</creatorcontrib><creatorcontrib>OHNISHI, TAKEO</creatorcontrib><title>The BRCA2 gene is a potential molecular target during 5-fluorouracil therapy in human oral cancer cells</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>5-Fluorouracil (5-FU) is widely used in clinical cancer therapy. It is commonly used either alone or in combination with other drugs and/or radiation for head and neck, and other types of cancers. 5-FU induces DNA double-strand breaks (DSBs). Inhibition of the repair of 5-FU-induced DSBs may improve the therapeutic response in many tumors to this anticancer agent. The aim of the present study was to further our understanding of the pathways which are involved in the repair of 5-FU-induced DSBs. Cell survival after drug treatment was examined with colony forming assays using Chinese hamster lung fibroblast cells or Chinese hamster ovary cell lines which are deficient in DSB repair pathways involving the homologous recombination repair-related genes BRCA2 and XRCC2, and the non-homologous end joining repair-related genes DNA-PKcs and Ku80. It was found that BRCA2 was involved in such repair, and may be effectively targeted to inhibit the repair of 5-FU-induced damage. Observations showed that knockdown of BRCA2 using small interference RNA suppression increased the sensitivity to 5-FU of human oral cancer cell lines (SAS and HSC3). These findings suggest that downregulation of BRCA2 may be useful for sensitizing tumor cells during 5-FU chemotherapy.</description><subject>5-fluorouracil</subject><subject>Animals</subject><subject>Antimetabolites, Antineoplastic - pharmacology</subject><subject>BRCA2</subject><subject>BRCA2 Protein - genetics</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell Survival - drug effects</subject><subject>Chemotherapy</subject><subject>CHO Cells</subject><subject>Cricetinae</subject><subject>Cricetulus</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Breaks, Double-Stranded - drug effects</subject><subject>DNA repair</subject><subject>DNA Repair - drug effects</subject><subject>double-strand breaks</subject><subject>Enzymes</subject><subject>Fibroblasts</subject><subject>Flow cytometry</subject><subject>Fluorouracil - pharmacology</subject><subject>Humans</subject><subject>M Phase Cell Cycle Checkpoints - drug effects</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Mouth Neoplasms - drug therapy</subject><subject>Mouth Neoplasms - genetics</subject><subject>Oral cancer</subject><subject>oral cancer cells</subject><subject>Proteins</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering</subject><subject>Rodents</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkc2LFDEQxYMo7rp68ywBQTyYMZWv7j6ug1-wIMgK3kI6XZnppTtpk-7D_vdmmHUPnuodfvWoV4-Q18B3su3Ex5R3goPaSd7yJ-QSmg6YUBKeVs0FMCn17wvyopQ7zkXDTfecXAhlqlTikhxuj0g__dxfC3rAiHQs1NElrRjX0U10ThP6bXKZri4fcKXDlsd4oJqFaUs5bdn5caLrEbNb7ukY6XGbXaQp12XvosdMPU5TeUmeBTcVfPUwr8ivL59v99_YzY-v3_fXN8wrrVYmG65VkK7HttUAQsvQoAhD6GTfKtH10gH2xgQ0ftCe68b1Qfm-NSBrIpBX5P3Zd8npz4ZltfNYThe4iGkrFjRIrkGYtqJv_0Pvap5Yr7PQSWEaAGkq9eFM-ZxKyRjsksfZ5XsL3J4KsCnbUwH2VEDF3zyYbv2MwyP87-MVeHcGyuLiMA6pPDIpMwmMayZ4TfIXQzGMIA</recordid><startdate>20140501</startdate><enddate>20140501</enddate><creator>NAKAGAWA, YOSUKE</creator><creator>KAJIHARA, ATSUHISA</creator><creator>TAKAHASHI, AKIHISA</creator><creator>KONDO, NATSUKO</creator><creator>MORI, EIICHIRO</creator><creator>KIRITA, TADAAKI</creator><creator>OHNISHI, TAKEO</creator><general>D.A. Spandidos</general><general>Spandidos Publications UK Ltd</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20140501</creationdate><title>The BRCA2 gene is a potential molecular target during 5-fluorouracil therapy in human oral cancer cells</title><author>NAKAGAWA, YOSUKE ; KAJIHARA, ATSUHISA ; TAKAHASHI, AKIHISA ; KONDO, NATSUKO ; MORI, EIICHIRO ; KIRITA, TADAAKI ; OHNISHI, TAKEO</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-37054f3abe88511253f7e2fdf93b8429b3a1eb66fe6cd5c057abf4cb861327013</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>5-fluorouracil</topic><topic>Animals</topic><topic>Antimetabolites, Antineoplastic - pharmacology</topic><topic>BRCA2</topic><topic>BRCA2 Protein - genetics</topic><topic>Cancer therapies</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Cell Survival - drug effects</topic><topic>Chemotherapy</topic><topic>CHO Cells</topic><topic>Cricetinae</topic><topic>Cricetulus</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Breaks, Double-Stranded - drug effects</topic><topic>DNA repair</topic><topic>DNA Repair - drug effects</topic><topic>double-strand breaks</topic><topic>Enzymes</topic><topic>Fibroblasts</topic><topic>Flow cytometry</topic><topic>Fluorouracil - pharmacology</topic><topic>Humans</topic><topic>M Phase Cell Cycle Checkpoints - drug effects</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Mice</topic><topic>Mouth Neoplasms - drug therapy</topic><topic>Mouth Neoplasms - genetics</topic><topic>Oral cancer</topic><topic>oral cancer cells</topic><topic>Proteins</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering</topic><topic>Rodents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>NAKAGAWA, YOSUKE</creatorcontrib><creatorcontrib>KAJIHARA, ATSUHISA</creatorcontrib><creatorcontrib>TAKAHASHI, AKIHISA</creatorcontrib><creatorcontrib>KONDO, NATSUKO</creatorcontrib><creatorcontrib>MORI, EIICHIRO</creatorcontrib><creatorcontrib>KIRITA, TADAAKI</creatorcontrib><creatorcontrib>OHNISHI, TAKEO</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>NAKAGAWA, YOSUKE</au><au>KAJIHARA, ATSUHISA</au><au>TAKAHASHI, AKIHISA</au><au>KONDO, NATSUKO</au><au>MORI, EIICHIRO</au><au>KIRITA, TADAAKI</au><au>OHNISHI, TAKEO</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The BRCA2 gene is a potential molecular target during 5-fluorouracil therapy in human oral cancer cells</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2014-05-01</date><risdate>2014</risdate><volume>31</volume><issue>5</issue><spage>2001</spage><epage>2006</epage><pages>2001-2006</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>5-Fluorouracil (5-FU) is widely used in clinical cancer therapy. It is commonly used either alone or in combination with other drugs and/or radiation for head and neck, and other types of cancers. 5-FU induces DNA double-strand breaks (DSBs). Inhibition of the repair of 5-FU-induced DSBs may improve the therapeutic response in many tumors to this anticancer agent. The aim of the present study was to further our understanding of the pathways which are involved in the repair of 5-FU-induced DSBs. Cell survival after drug treatment was examined with colony forming assays using Chinese hamster lung fibroblast cells or Chinese hamster ovary cell lines which are deficient in DSB repair pathways involving the homologous recombination repair-related genes BRCA2 and XRCC2, and the non-homologous end joining repair-related genes DNA-PKcs and Ku80. It was found that BRCA2 was involved in such repair, and may be effectively targeted to inhibit the repair of 5-FU-induced damage. Observations showed that knockdown of BRCA2 using small interference RNA suppression increased the sensitivity to 5-FU of human oral cancer cell lines (SAS and HSC3). These findings suggest that downregulation of BRCA2 may be useful for sensitizing tumor cells during 5-FU chemotherapy.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>24627042</pmid><doi>10.3892/or.2014.3080</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 5-fluorouracil Animals Antimetabolites, Antineoplastic - pharmacology BRCA2 BRCA2 Protein - genetics Cancer therapies Cell cycle Cell Line, Tumor Cell Survival - drug effects Chemotherapy CHO Cells Cricetinae Cricetulus Deoxyribonucleic acid DNA DNA Breaks, Double-Stranded - drug effects DNA repair DNA Repair - drug effects double-strand breaks Enzymes Fibroblasts Flow cytometry Fluorouracil - pharmacology Humans M Phase Cell Cycle Checkpoints - drug effects Metabolism Metabolites Mice Mouth Neoplasms - drug therapy Mouth Neoplasms - genetics Oral cancer oral cancer cells Proteins RNA Interference RNA, Small Interfering Rodents |
| title | The BRCA2 gene is a potential molecular target during 5-fluorouracil therapy in human oral cancer cells |
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