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An essential role for protein synthesis in oncogenic cellular transformation

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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Correspondence to Andreas G Bader.

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Bader, A., Vogt, P. An essential role for protein synthesis in oncogenic cellular transformation. Oncogene 23, 3145–3150 (2004). https://doi.org/10.1038/sj.onc.1207550

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