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Chromosome 20q Amplification Regulates in Vitro Response to Kinesin-5 Inhibitor

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Publication Date: 26 Mar 2008

Journal: Cancer Informatics 2008:6 147-164

CI
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Abstract Aimee L. Jackson*1, Mao Mao*1, Sumire Kobayashi1, Teresa Ward1, Matthew Biery1, Hongyue Dai1, Steven R. Bartz2 and Peter S. Linsley1

1Rosetta Inpharmatics LLC, a wholly-owned subsidiary of Merck and Co., Inc., Seattle, WA 98109. 2Sirna Therapeutics, a wholly-owned subsidiary of Merck and Co., Inc., San Francisco, CA 94158.

*These two authors contributed equally to this work.

Abstract

We identified gene expression signatures predicting responsiveness to a Kinesin-5 (KIF11) inhibitor (Kinesin-5i) in cultured colon tumor cell lines. Genes predicting resistance to Kinesin-5i were enriched for those from chromosome 20q, a region of frequent amplifi cation in a number of tumor types. siRNAs targeting genes in this chromosomal region identified AURKA, TPX2 and MYBL2 as genes whose disruption enhances response to Kinesin-5i. Taken together, our results show functional interaction between these genes, and suggest that their overexpression is involved in resistance to Kinesin-5i. Furthermore, our results suggest that patients whose tumors overexpress AURKA due to amplification of 20q will more likely resist treatment with Kinesin-5 inhibitor, and that inactivation of AURKA may sensitize these patients to treatment.


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