Human RIF1 encodes an anti-apoptotic factor required for DNA repair
Human Rap1-interacting protein 1 (RIF1) contributes to the ataxia telangiectasia, mutated-mediated DNA damage response against the dexterous effect of DNA lesions and plays a critical role in the S-phase checkpoint. However, the molecular mechanisms by which human RIF1 conquers DNA aberrations remai...
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Veröffentlicht in: | Carcinogenesis (New York) 2009-08, Vol.30 (8), p.1314-1319 |
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creator | Wang, Haibo Zhao, Ailian Chen, Lin Zhong, Xueyan Liao, Ji Gao, Min Cai, Minghua Lee, Dong-Hyun Li, Jing Chowdhury, Dipanjan Yang, Yun-gui Pfeifer, Gerd P. Yen, Yun Xu, Xingzhi |
description | Human Rap1-interacting protein 1 (RIF1) contributes to the ataxia telangiectasia, mutated-mediated DNA damage response against the dexterous effect of DNA lesions and plays a critical role in the S-phase checkpoint. However, the molecular mechanisms by which human RIF1 conquers DNA aberrations remain largely unknown. We here showed that inhibition of RIF1 expression by small interfering RNA led to defective homologous recombination-mediated DNA double-strand break repair and sensitized cancer cells to camptothecin or staurosporine treatment. RIF1 underwent caspase-dependent cleavage upon apoptosis. We further found that RIF1 was highly expressed in human breast tumors, and its expression status was positively correlated with differentiation degrees of invasive ductal carcinoma of the breast. Our results suggest that RIF1 encodes an anti-apoptotic factor required for DNA repair and is a potential target for cancer treatment. |
doi_str_mv | 10.1093/carcin/bgp136 |
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However, the molecular mechanisms by which human RIF1 conquers DNA aberrations remain largely unknown. We here showed that inhibition of RIF1 expression by small interfering RNA led to defective homologous recombination-mediated DNA double-strand break repair and sensitized cancer cells to camptothecin or staurosporine treatment. RIF1 underwent caspase-dependent cleavage upon apoptosis. We further found that RIF1 was highly expressed in human breast tumors, and its expression status was positively correlated with differentiation degrees of invasive ductal carcinoma of the breast. Our results suggest that RIF1 encodes an anti-apoptotic factor required for DNA repair and is a potential target for cancer treatment.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/bgp136</identifier><identifier>PMID: 19483192</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Apoptosis - drug effects ; Biological and medical sciences ; Blotting, Western ; Breast Neoplasms - drug therapy ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Camptothecin - therapeutic use ; Cancer Biology ; Carcinogenesis, carcinogens and anticarcinogens ; Carcinoma, Ductal, Breast - drug therapy ; Carcinoma, Ductal, Breast - metabolism ; Carcinoma, Ductal, Breast - pathology ; Cell Differentiation ; Cell Proliferation ; DNA Breaks, Double-Stranded ; DNA Repair ; Enzyme Inhibitors - pharmacology ; Female ; Humans ; Immunoenzyme Techniques ; Immunoprecipitation ; Medical sciences ; Nuclear Proteins - physiology ; Nuclear Receptor Co-Repressor 1 ; Repressor Proteins - physiology ; RNA, Small Interfering - pharmacology ; Signal Transduction - drug effects ; Staurosporine - therapeutic use ; Tumor Cells, Cultured ; Tumors</subject><ispartof>Carcinogenesis (New York), 2009-08, Vol.30 (8), p.1314-1319</ispartof><rights>The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org 2009</rights><rights>2009 INIST-CNRS</rights><rights>The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c544t-404b40ee9663f556cc77e9cc874264ab7df38c9c0ba25859d8ae9f0f4e5422a73</citedby><cites>FETCH-LOGICAL-c544t-404b40ee9663f556cc77e9cc874264ab7df38c9c0ba25859d8ae9f0f4e5422a73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,1584,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21798650$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19483192$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Haibo</creatorcontrib><creatorcontrib>Zhao, Ailian</creatorcontrib><creatorcontrib>Chen, Lin</creatorcontrib><creatorcontrib>Zhong, Xueyan</creatorcontrib><creatorcontrib>Liao, Ji</creatorcontrib><creatorcontrib>Gao, Min</creatorcontrib><creatorcontrib>Cai, Minghua</creatorcontrib><creatorcontrib>Lee, Dong-Hyun</creatorcontrib><creatorcontrib>Li, Jing</creatorcontrib><creatorcontrib>Chowdhury, Dipanjan</creatorcontrib><creatorcontrib>Yang, Yun-gui</creatorcontrib><creatorcontrib>Pfeifer, Gerd P.</creatorcontrib><creatorcontrib>Yen, Yun</creatorcontrib><creatorcontrib>Xu, Xingzhi</creatorcontrib><title>Human RIF1 encodes an anti-apoptotic factor required for DNA repair</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>Human Rap1-interacting protein 1 (RIF1) contributes to the ataxia telangiectasia, mutated-mediated DNA damage response against the dexterous effect of DNA lesions and plays a critical role in the S-phase checkpoint. However, the molecular mechanisms by which human RIF1 conquers DNA aberrations remain largely unknown. We here showed that inhibition of RIF1 expression by small interfering RNA led to defective homologous recombination-mediated DNA double-strand break repair and sensitized cancer cells to camptothecin or staurosporine treatment. RIF1 underwent caspase-dependent cleavage upon apoptosis. We further found that RIF1 was highly expressed in human breast tumors, and its expression status was positively correlated with differentiation degrees of invasive ductal carcinoma of the breast. Our results suggest that RIF1 encodes an anti-apoptotic factor required for DNA repair and is a potential target for cancer treatment.</description><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Camptothecin - therapeutic use</subject><subject>Cancer Biology</subject><subject>Carcinogenesis, carcinogens and anticarcinogens</subject><subject>Carcinoma, Ductal, Breast - drug therapy</subject><subject>Carcinoma, Ductal, Breast - metabolism</subject><subject>Carcinoma, Ductal, Breast - pathology</subject><subject>Cell Differentiation</subject><subject>Cell Proliferation</subject><subject>DNA Breaks, Double-Stranded</subject><subject>DNA Repair</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Female</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Immunoprecipitation</subject><subject>Medical sciences</subject><subject>Nuclear Proteins - physiology</subject><subject>Nuclear Receptor Co-Repressor 1</subject><subject>Repressor Proteins - physiology</subject><subject>RNA, Small Interfering - pharmacology</subject><subject>Signal Transduction - drug effects</subject><subject>Staurosporine - therapeutic use</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0d9r1TAUB_AgirtOH32VIii-1OVXk-ZlMO-cd7BNkIniSzhN05nZm3RJO-Z_b0bL9ceLT-EkH05O8kXoOcFvCVbswEA0zh80VwNh4gFaES5wSUmNH6IVJpyVjDG-h56kdI0xEaxSj9EeUbxmRNEVWm-mLfji0-kJKaw3obWpyDX40ZUwhGEMozNFB2YMsYj2ZnLRtkWXi-OLo7wxgItP0aMO-mSfLes--nzy_nK9Kc8-fjhdH52VpuJ8LDnmDcfWKiFYV1XCGCmtMqaWnAoOjWw7VhtlcAO0qivV1mBVhztuK04pSLaPDue-w9RsbWusHyP0eohuC_GnDuD03yfefddX4VZTmf9D3jd4vTSI4WayadRbl4zte_A2TElTLBUllGf48h94Habo8-M0JYoxwhXJqJyRiSGlaLvdJATr-2z0nI2es8n-xZ_j_9ZLGBm8WgAkA30XwRuXdo4SqWpR4ezezC5Mw3_vXGZ0abR3OwzxhxaSyUpvvn7Tx-fv6vOLL5dasF8IFrWC</recordid><startdate>20090801</startdate><enddate>20090801</enddate><creator>Wang, Haibo</creator><creator>Zhao, Ailian</creator><creator>Chen, Lin</creator><creator>Zhong, Xueyan</creator><creator>Liao, Ji</creator><creator>Gao, Min</creator><creator>Cai, Minghua</creator><creator>Lee, Dong-Hyun</creator><creator>Li, Jing</creator><creator>Chowdhury, Dipanjan</creator><creator>Yang, Yun-gui</creator><creator>Pfeifer, Gerd P.</creator><creator>Yen, Yun</creator><creator>Xu, Xingzhi</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><scope>IQODW</scope><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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20090801</creationdate><title>Human RIF1 encodes an anti-apoptotic factor required for DNA repair</title><author>Wang, Haibo ; Zhao, Ailian ; Chen, Lin ; Zhong, Xueyan ; Liao, Ji ; Gao, Min ; Cai, Minghua ; Lee, Dong-Hyun ; Li, Jing ; Chowdhury, Dipanjan ; Yang, Yun-gui ; Pfeifer, Gerd P. ; Yen, Yun ; Xu, Xingzhi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c544t-404b40ee9663f556cc77e9cc874264ab7df38c9c0ba25859d8ae9f0f4e5422a73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Camptothecin - therapeutic use</topic><topic>Cancer Biology</topic><topic>Carcinogenesis, carcinogens and anticarcinogens</topic><topic>Carcinoma, Ductal, Breast - drug therapy</topic><topic>Carcinoma, Ductal, Breast - metabolism</topic><topic>Carcinoma, Ductal, Breast - pathology</topic><topic>Cell Differentiation</topic><topic>Cell Proliferation</topic><topic>DNA Breaks, Double-Stranded</topic><topic>DNA Repair</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Female</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>Immunoprecipitation</topic><topic>Medical sciences</topic><topic>Nuclear Proteins - physiology</topic><topic>Nuclear Receptor Co-Repressor 1</topic><topic>Repressor Proteins - physiology</topic><topic>RNA, Small Interfering - pharmacology</topic><topic>Signal Transduction - drug effects</topic><topic>Staurosporine - therapeutic use</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Haibo</creatorcontrib><creatorcontrib>Zhao, Ailian</creatorcontrib><creatorcontrib>Chen, Lin</creatorcontrib><creatorcontrib>Zhong, Xueyan</creatorcontrib><creatorcontrib>Liao, Ji</creatorcontrib><creatorcontrib>Gao, Min</creatorcontrib><creatorcontrib>Cai, Minghua</creatorcontrib><creatorcontrib>Lee, Dong-Hyun</creatorcontrib><creatorcontrib>Li, Jing</creatorcontrib><creatorcontrib>Chowdhury, Dipanjan</creatorcontrib><creatorcontrib>Yang, Yun-gui</creatorcontrib><creatorcontrib>Pfeifer, Gerd P.</creatorcontrib><creatorcontrib>Yen, Yun</creatorcontrib><creatorcontrib>Xu, Xingzhi</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Haibo</au><au>Zhao, Ailian</au><au>Chen, Lin</au><au>Zhong, Xueyan</au><au>Liao, Ji</au><au>Gao, Min</au><au>Cai, Minghua</au><au>Lee, Dong-Hyun</au><au>Li, Jing</au><au>Chowdhury, Dipanjan</au><au>Yang, Yun-gui</au><au>Pfeifer, Gerd P.</au><au>Yen, Yun</au><au>Xu, Xingzhi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Human RIF1 encodes an anti-apoptotic factor required for DNA repair</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>2009-08-01</date><risdate>2009</risdate><volume>30</volume><issue>8</issue><spage>1314</spage><epage>1319</epage><pages>1314-1319</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><abstract>Human Rap1-interacting protein 1 (RIF1) contributes to the ataxia telangiectasia, mutated-mediated DNA damage response against the dexterous effect of DNA lesions and plays a critical role in the S-phase checkpoint. However, the molecular mechanisms by which human RIF1 conquers DNA aberrations remain largely unknown. We here showed that inhibition of RIF1 expression by small interfering RNA led to defective homologous recombination-mediated DNA double-strand break repair and sensitized cancer cells to camptothecin or staurosporine treatment. RIF1 underwent caspase-dependent cleavage upon apoptosis. We further found that RIF1 was highly expressed in human breast tumors, and its expression status was positively correlated with differentiation degrees of invasive ductal carcinoma of the breast. Our results suggest that RIF1 encodes an anti-apoptotic factor required for DNA repair and is a potential target for cancer treatment.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>19483192</pmid><doi>10.1093/carcin/bgp136</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Apoptosis - drug effects Biological and medical sciences Blotting, Western Breast Neoplasms - drug therapy Breast Neoplasms - metabolism Breast Neoplasms - pathology Camptothecin - therapeutic use Cancer Biology Carcinogenesis, carcinogens and anticarcinogens Carcinoma, Ductal, Breast - drug therapy Carcinoma, Ductal, Breast - metabolism Carcinoma, Ductal, Breast - pathology Cell Differentiation Cell Proliferation DNA Breaks, Double-Stranded DNA Repair Enzyme Inhibitors - pharmacology Female Humans Immunoenzyme Techniques Immunoprecipitation Medical sciences Nuclear Proteins - physiology Nuclear Receptor Co-Repressor 1 Repressor Proteins - physiology RNA, Small Interfering - pharmacology Signal Transduction - drug effects Staurosporine - therapeutic use Tumor Cells, Cultured Tumors |
title | Human RIF1 encodes an anti-apoptotic factor required for DNA repair |
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