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Loss of PI3K blocks cell-cycle progression in a Drosophila tumor model

Abstract

Tumorigenesis is a complex process, which requires alterations in several tumor suppressor or oncogenes. Here, we use a Drosophila tumor model to identify genes, which are specifically required for tumor growth. We found that reduction of phosphoinositide 3-kinase (PI3K) activity resulted in very small tumors while only slightly affecting growth of wild-type tissue. The observed inhibition on tumor growth occurred at the level of cell-cycle progression. We conclude that tumor cells become dependent on PI3K function and that reduction of PI3K activity synthetically interferes with tumor growth. The results presented here broaden our insights into the intricate mechanisms underling tumorigenesis and illustrate the power of Drosophila genetics in revealing weak points of tumor progression.

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Acknowledgements

We would like to thank G Hausmann and J Zartman for comments on the manuscript; A Smith for help with experiments; and H Stocker, the Bloomington Stock Center, the National Institute of Genetics (NIG) and the Vienna Drosophila RNAi Center (VDRC) for fly strains. This work was supported by an FEBS Long-term Fellowship to MW, the Swiss National Science Foundation and the Kanton of Zurich.

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Correspondence to K Basler.

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Willecke, M., Toggweiler, J. & Basler, K. Loss of PI3K blocks cell-cycle progression in a Drosophila tumor model. Oncogene 30, 4067–4074 (2011). https://doi.org/10.1038/onc.2011.125

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