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Horizon Discovery X‐MAN™ cell lines reveal how PI3K mutation can result in EMT switch and increased invasiveness
Sue Griffin1, Jeffrey Wallin2, Jane Guan2, Kyle Edgar2, Wei Zhou2, Ross Francis2, Anthony Torres2, Peter Haverty3, Jeffrey Eastham‐Anderson4, Sabrina Arena5, Alberto Bardelli5,6, John Goodall1, Kyla Grimshaw1, Klaus Hoeflich2, Marcia Belvin2, Lori Friedman2 and Christopher Torrance1
Horizon Discovery Ltd., Cambridge, UK1, Departments of Cancer Signaling and Translational Oncology2, Bioinformatics3, Pathology4, Genentech, Inc., South San Francisco, CA, USA
Laboratory of Molecular Genetics, Institute for Cancer Research and Treatment, University of Torino Medical School, Candiolo, Italy5
FIRC Institute of Molecular Oncology, Via Adamello 16, Milan, ZIP 20139, Italy6
Sponsored by Horizon Discovery Ltd.
A major challenge facing the development of PI3K-targeted pharmaceutical agents is the lack of patient-relevant, in vitro model systems. Studies into the function of oncogenic mutations are commonly carried out in cell line panels that are mutant or wild-type for the gene of interest, however interpretation of these studies can be confounded by additional genetic differences between each cell line background, calling into question the reliability of the results.
Horizon Discovery’s proprietary rAAV GENESIS™ technology directly addresses this problem through the development of X-MAN™ isogenic cell lines. These models allow the interrogation of protein function without the problems associated with protein over-expression studies or genetically diverse cell line panels.
In order to investigate the effect that a PI3K mutation might have on tumour development, we employed isogenic cell lines derived from a ‘normal’ background. A PI3Kα (H1047R) mutation (commonly found in breast cancer patients) was knocked-in to produce a pair of MCF10A cell lines; parental cells that express wild-type PI3K or PI3Kα (H1047R) cells that express mutant PI3K1.
This investigation highlights how Horizon’s rAAV GENESIS technology can be applied, and reveals that introduction of a PI3K activating mutation can result in EMT switch and increased cell invasiveness.
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