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KMID : 1140120080130030153
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Cancer Prevention Research
2008 Volume.13 No. 3 p.153 ~ p.161
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Regulation of Apoptosis by PI3K-PTEN-PKB/Akt Signaling Pathway
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Park Jae-Hyun
Choi Yung-Hyun
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Abstract
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Recently, the understanding of protein kinase B (PKB) activation and mechanisms for promoting cell survival has expanded rapidly. Several PKB substrates involved in apoptopsis have been described and many processes inhibiting cell death have been identified. In this context, the mitochondrion appears to be the key organelle in which PKB drives its anti-apoptotic activities. Additionally, by modulating transcription factor activity or inhibiting nucleus condensation/fragmentation, PKB interferes with upstream mitochondrial cell death signals, but it also maintains mitochondrial integrity by reinforcing the roles of key players acting on mitochondrial membranes. Moreover, caspase activity, which represents mitochondrial downstream events in the apoptotic process, can be prevented by PKB in different ways. More recent several studies have shown that mitochondria can also be fragmented in cells that normally undergo programmed cell death, supporting the notion that mitochondrial remodelling plays an important role in the process. The function of PKB is still not clear and further investigations of its possible role as a modulator of mitochondrial dynamics are required. This could lead to a major breakthrough in our understanding of PKB functions in cell survival and to the generation of powerful tools for cancer therapy. (Cancer Prev Res 13, 153-161, 2008)
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KEYWORD
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AKT/PKB, Mitochondria, Apoptosis
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