Abstract
The phosphatidyl inositol 3-kinase (PI3K)/Akt pathway is activated downstream of a variety of extracellular signals and activation of this signaling pathway impacts a number of cellular processes including cell growth, proliferation and survival. The alteration of components of this pathway, through either activation of oncogenes or inactivation of tumor suppressors, disrupts a signaling equilibrium and can thus lead to cellular transformation. The frequent dysregulation of the PI3K/Akt pathway in human cancer has made components of this pathway attractive for therapeutic targeting; however, a more comprehensive understanding of the signaling intricacies is necessary to develop pharmacological agents to target not only specific molecules, but also specific functions. Here, we review a series of experiments examining the contribution of molecules of this signaling network including PI3K, phosphatase and tensin homolog deleted on chromosome 10, integrin-linked kinase and Akt and address the significance to human breast cancer.
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Acknowledgements
WJM is supported by CRC Chair in Molecular Oncology. RLD is supported by a pre-doctoral award from the DOD. This work was supported by grants from NCI PPG #102036 and CBCRA awarded to WJM.
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Dillon, R., White, D. & Muller, W. The phosphatidyl inositol 3-kinase signaling network: implications for human breast cancer. Oncogene 26, 1338–1345 (2007). https://doi.org/10.1038/sj.onc.1210202
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DOI: https://doi.org/10.1038/sj.onc.1210202
Keywords
- PI3K
- Akt
- PTEN
- ILK
- breast cancer
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