Journal article
Differential SKIP expression in PTEN-deficient glioblastoma regulates cellular proliferation and migration
EM Davies, AM Kong, A Tan, R Gurung, A Sriratana, PE Bukczynska, LM Ooms, CA McLean, T Tiganis, CA Mitchell
Oncogene | NATURE PUBLISHING GROUP | Published : 2015
DOI: 10.1038/onc.2014.303
Abstract
Glioblastoma is the most common and lethal primary malignant brain tumor in adults. The tumor suppressor gene PTEN is deleted, mutated or hypermethylated in more than 60% of glioblastoma cases resulting in hyperactivation of the phosphoinositide 3-kinase pathway, which leads to sustained PI(3,4,5)P 3 signaling, and thereby hyperactivation of Akt and other effectors. PI(3,4,5)P 3 is also hydrolyzed to PI(3,4)P 2 by inositol polyphosphate 5-phosphatases such as SKIP, but the role this pathway has in glioblastoma is unknown. Microarray expression profiling of SKIP in human glioblastoma has revealed both increased and decreased SKIP gene expression. Here we have screened PTEN-deficient glioblast..
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Awarded by National Health and Medical Research Council
Funding Acknowledgements
We thank Dr Tamas Balla (NIH) for kindly providing the GFP-PH/Btk and GFP-PH/PLC delta constructs and Dr Jelena Becanovic for assistance with ONCOMINE data analysis. This work was supported by the National Health & Medical Research Council (NH&MRC), Australia, grant number 384083. We also thank the Biochemistry Imaging Facility, Department of Biochemistry and Molecular Biology, Monash University and the Monash Micro Imaging Facility for technical advice with image acquisition and analysis. Tony Tiganis is a NHMRC research fellow. The results shown here are in part based upon data generated by The Cancer Genome Atlas Research Network http://cancergenome.nih.gov/.