Abstract
The induction and maintenance of oncogenic transformation requires interference with the controls that regulate translation and transcription. The PI 3-kinase pathway, which shows gain of function in numerous and diverse human cancers, generates signals that have a positive effect on the initiation of protein synthesis. Here we review the components of the PI 3-kinase signaling pathway and the mRNA-binding protein YB-1, exploring their roles in protein synthesis and oncogenic cell transformation.
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Abbreviations
- BRCA1:
-
breast cancer susceptibility gene product
- eIF4E:
-
eucaryotic initiation factor 4E
- IκB:
-
inhibitor of NFκB
- IKK:
-
IκB kinase
- mRNP:
-
messenger ribonucleoprotein particle
- NFκB:
-
nuclear factor κB
- PI3K:
-
phosphoinositide 3-kinase
- PTEN:
-
phosphatase and tensin homolog deleted on chromosome 10
- Raptor:
-
regulatory associated protein of TOR
- Rheb:
-
Ras homolog enriched in brain
- TOR:
-
target of rapamycin
- TOS:
-
TOR signaling
- TSC:
-
tuberous sclerosis complex
- YB-1:
-
Y box-binding protein 1
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Acknowledgements
Research of the authors is supported by grants from the National Cancer Institute, National Institutes of Health and the Austrian Science Foundation (FWF). This is manuscript number 16175-MEM from The Scripps Research Institute.
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