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

10:15 EDT 22nd September 2014 | BioPortfolio

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

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.Oncogene advance online publication, 25 April 2011; doi:10.1038/onc.2011.125.

Affiliation

Institute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.

Journal Details

This article was published in the following journal.

Name: Oncogene
ISSN: 1476-5594
Pages:

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Medical and Biotech [MESH] Definitions

Proteins whose abnormal expression (gain or loss) are associated with the development, growth, or progression of NEOPLASMS. Some neoplasm proteins are tumor antigens (ANTIGENS, NEOPLASM), i.e. they induce an immune reaction to their tumor. Many neoplasm proteins have been characterized and are used as tumor markers (TUMOR MARKERS, BIOLOGICAL) when they are detectable in cells and body fluids as monitors for the presence or growth of tumors. Abnormal expression of ONCOGENE PROTEINS is involved in neoplastic transformation, whereas the loss of expression of TUMOR SUPPRESSOR PROTEINS is involved with the loss of growth control and progression of the neoplasm.

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