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Ribosomal protein S11 influences glioma response to TOP2 poisons. 2020
Chidiebere U Awah, and
Li Chen, and
Mukesh Bansal, and
Aayushi Mahajan, and
Jan Winter, and
Meeki Lad, and
Louisa Warnke, and
Edgar Gonzalez-Buendia, and
Cheol Park, and
Daniel Zhang, and
Eric Feldstein, and
Dou Yu, and
Markella Zannikou, and
Irina V Balyasnikova, and
Regina Martuscello, and
Silvana Konerman, and
Balázs Győrffy, and
Kirsten B Burdett, and
Denise M Scholtens, and
Roger Stupp, and
Atique Ahmed, and
Patrick Hsu, and
Adam M Sonabend
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University , Chicago, IL, United States.
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.
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