Oncogenic PI3K deregulates transcription and translation.
There have long been indications of a role for PI3K (phosphatidylinositol 3-kinase) in cancer pathogenesis. Experimental data document a requirement for deregulation of both transcription and translation in PI3K-mediated oncogenic transformation. The recent discoveries of cancer-specific mutations in PIK3CA, the gene that encodes the catalytic subunit p110alpha of PI3K, have heightened the interest in the oncogenic potential of this lipid kinase and have made p110alpha an ideal drug target.
Bader
Andreas G
AG
Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA.
Kang
Sohye
S
Zhao
Li
L
Vogt
Peter K
PK
D020134:Catalytic Domain; D051858:Forkhead Transcription Factors / Q000235:genetics; D006801:Humans; D009154:Mutation; D009369:Neoplasms / Q000201:enzymology* / Q000235:genetics; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics*; D000081082:Phosphoinositide-3 Kinase Inhibitors; D014176:Protein Biosynthesis; D021382:Protein Sorting Signals / Q000235:genetics; D014158:Transcription, Genetic
D051858:Forkhead Transcription Factors; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D021382:Protein Sorting Signals