Ribosomal protein S11 influences glioma response to TOP2 poisons
Topoisomerase II poisons are one of the most common class of chemotherapeutics used in cancer. We and others had shown that a subset of glioblastomas, the most malignant of all primary brain tumors in adults, is responsive to TOP2 poisons. To identify genes that confer susceptibility to this drug in...
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| Veröffentlicht in: | Oncogene 2020-07, Vol.39 (27), p.5068-5081 |
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| creator | Awah, Chidiebere U. Chen, Li Bansal, Mukesh Mahajan, Aayushi Winter, Jan Lad, Meeki Warnke, Louisa Gonzalez-Buendia, Edgar Park, Cheol Zhang, Daniel Feldstein, Eric Yu, Dou Zannikou, Markella Balyasnikova, Irina V. Martuscello, Regina Konerman, Silvana Győrffy, Balázs Burdett, Kirsten B. Scholtens, Denise M. Stupp, Roger Ahmed, Atique Hsu, Patrick Sonabend, Adam M. |
| description | Topoisomerase II poisons are one of the most common class of chemotherapeutics used in cancer. We and others had shown that a subset of glioblastomas, the most malignant of all primary brain tumors in adults, is responsive to TOP2 poisons. To identify genes that confer susceptibility to this drug in gliomas, we performed a genome-scale CRISPR knockout screen with etoposide. Genes involved in protein synthesis and DNA damage were implicated in etoposide susceptibility. To define potential biomarkers for TOP2 poisons, CRISPR hits were overlapped with genes whose expression correlates with susceptibility to this drug across glioma cell lines, revealing ribosomal protein subunit RPS11, 16, and 18 as putative biomarkers for response to TOP2 poisons. Loss of RPS11 led to resistance to etoposide and doxorubicin and impaired the induction of proapoptotic gene APAF1 following treatment. The expression of these ribosomal subunits was also associated with susceptibility to TOP2 poisons across cell lines from gliomas and multiple other cancers. |
| doi_str_mv | 10.1038/s41388-020-1342-0 |
| format | Article |
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We and others had shown that a subset of glioblastomas, the most malignant of all primary brain tumors in adults, is responsive to TOP2 poisons. To identify genes that confer susceptibility to this drug in gliomas, we performed a genome-scale CRISPR knockout screen with etoposide. Genes involved in protein synthesis and DNA damage were implicated in etoposide susceptibility. To define potential biomarkers for TOP2 poisons, CRISPR hits were overlapped with genes whose expression correlates with susceptibility to this drug across glioma cell lines, revealing ribosomal protein subunit RPS11, 16, and 18 as putative biomarkers for response to TOP2 poisons. Loss of RPS11 led to resistance to etoposide and doxorubicin and impaired the induction of proapoptotic gene APAF1 following treatment. The expression of these ribosomal subunits was also associated with susceptibility to TOP2 poisons across cell lines from gliomas and multiple other cancers.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/s41388-020-1342-0</identifier><identifier>PMID: 32528131</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/67/1922 ; 692/53/2423 ; Apoptosis ; Biological markers ; Biomarkers ; Brain cancer ; Brain tumors ; Care and treatment ; Cell Biology ; CRISPR ; Development and progression ; DNA biosynthesis ; DNA damage ; DNA topoisomerase (ATP-hydrolysing) ; Doxorubicin ; Etoposide ; Gene expression ; Genetic aspects ; Genomes ; Glioma ; Glioma cells ; Gliomas ; Health aspects ; Human Genetics ; Identification and classification ; Internal Medicine ; Medicine ; Medicine & Public Health ; Oncology ; Protein biosynthesis ; Proteins ; Ribosomal protein S11 ; Ribosomal subunits ; Susceptibility ; Topoisomerases</subject><ispartof>Oncogene, 2020-07, Vol.39 (27), p.5068-5081</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Limited 2020</rights><rights>COPYRIGHT 2020 Nature Publishing Group</rights><rights>The Author(s), under exclusive licence to Springer Nature Limited 2020.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c542t-ebda41500521f276bfdd8150df96aee29254cd05d23587309c587440ac91af03</citedby><cites>FETCH-LOGICAL-c542t-ebda41500521f276bfdd8150df96aee29254cd05d23587309c587440ac91af03</cites><orcidid>0000-0002-5483-3118 ; 0000-0001-9962-9295 ; 0000-0002-8347-1945</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41388-020-1342-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41388-020-1342-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27903,27904,41467,42536,51297</link.rule.ids></links><search><creatorcontrib>Awah, Chidiebere U.</creatorcontrib><creatorcontrib>Chen, Li</creatorcontrib><creatorcontrib>Bansal, Mukesh</creatorcontrib><creatorcontrib>Mahajan, Aayushi</creatorcontrib><creatorcontrib>Winter, Jan</creatorcontrib><creatorcontrib>Lad, Meeki</creatorcontrib><creatorcontrib>Warnke, Louisa</creatorcontrib><creatorcontrib>Gonzalez-Buendia, Edgar</creatorcontrib><creatorcontrib>Park, Cheol</creatorcontrib><creatorcontrib>Zhang, Daniel</creatorcontrib><creatorcontrib>Feldstein, Eric</creatorcontrib><creatorcontrib>Yu, Dou</creatorcontrib><creatorcontrib>Zannikou, Markella</creatorcontrib><creatorcontrib>Balyasnikova, Irina V.</creatorcontrib><creatorcontrib>Martuscello, Regina</creatorcontrib><creatorcontrib>Konerman, Silvana</creatorcontrib><creatorcontrib>Győrffy, Balázs</creatorcontrib><creatorcontrib>Burdett, Kirsten B.</creatorcontrib><creatorcontrib>Scholtens, Denise M.</creatorcontrib><creatorcontrib>Stupp, Roger</creatorcontrib><creatorcontrib>Ahmed, Atique</creatorcontrib><creatorcontrib>Hsu, Patrick</creatorcontrib><creatorcontrib>Sonabend, Adam M.</creatorcontrib><title>Ribosomal protein S11 influences glioma response to TOP2 poisons</title><title>Oncogene</title><addtitle>Oncogene</addtitle><description>Topoisomerase II poisons are one of the most common class of chemotherapeutics used in cancer. We and others had shown that a subset of glioblastomas, the most malignant of all primary brain tumors in adults, is responsive to TOP2 poisons. To identify genes that confer susceptibility to this drug in gliomas, we performed a genome-scale CRISPR knockout screen with etoposide. Genes involved in protein synthesis and DNA damage were implicated in etoposide susceptibility. To define potential biomarkers for TOP2 poisons, CRISPR hits were overlapped with genes whose expression correlates with susceptibility to this drug across glioma cell lines, revealing ribosomal protein subunit RPS11, 16, and 18 as putative biomarkers for response to TOP2 poisons. Loss of RPS11 led to resistance to etoposide and doxorubicin and impaired the induction of proapoptotic gene APAF1 following treatment. The expression of these ribosomal subunits was also associated with susceptibility to TOP2 poisons across cell lines from gliomas and multiple other cancers.</description><subject>631/67/1922</subject><subject>692/53/2423</subject><subject>Apoptosis</subject><subject>Biological markers</subject><subject>Biomarkers</subject><subject>Brain cancer</subject><subject>Brain tumors</subject><subject>Care and treatment</subject><subject>Cell Biology</subject><subject>CRISPR</subject><subject>Development and progression</subject><subject>DNA biosynthesis</subject><subject>DNA damage</subject><subject>DNA topoisomerase (ATP-hydrolysing)</subject><subject>Doxorubicin</subject><subject>Etoposide</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Glioma</subject><subject>Glioma cells</subject><subject>Gliomas</subject><subject>Health aspects</subject><subject>Human Genetics</subject><subject>Identification and 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| subjects | 631/67/1922 692/53/2423 Apoptosis Biological markers Biomarkers Brain cancer Brain tumors Care and treatment Cell Biology CRISPR Development and progression DNA biosynthesis DNA damage DNA topoisomerase (ATP-hydrolysing) Doxorubicin Etoposide Gene expression Genetic aspects Genomes Glioma Glioma cells Gliomas Health aspects Human Genetics Identification and classification Internal Medicine Medicine Medicine & Public Health Oncology Protein biosynthesis Proteins Ribosomal protein S11 Ribosomal subunits Susceptibility Topoisomerases |
| title | Ribosomal protein S11 influences glioma response to TOP2 poisons |
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