Regulation in Cell Cycle via p53 and PTEN Tumor Suppressors
DOI:
https://doi.org/10.17140/CSMMOJ-1-101Keywords:
p53, PTEN, AKT, MDM2, Protein interaction, Protein degradation, Cell signaling, Cell cycle regulationAbstract
One of the target effectors of p53 transcription factor is the Phosphatase and Tensin homologue deleted on chromosome 10 (PTEN) which has protein phosphatase activity and lipid phosphatase activity that antagonizes PI3K activity. Cells that lack PTEN have constitutively higher levels of PIP3 and activated downstream targets. Both p53 and PTEN are tumor suppressors that act by inhibiting cell cycle progression and promoting apoptosis. Germline mutations in p53 and PTEN cause Li-Fraumeni syndrome and Cowden syndrome, respectively. The p53 cooperates with PTEN, which might be an essential blockage in development of cancers. PTEN protects p53 from MDM2-mediated degradation, whereas p53 can enhance the transcription of PTEN. This review summarizes the function of PTEN and p53 in cell cycle regulation. We will also discuss the role of PTEN signaling through its interaction with p53 and MDM2 pathways for the potential implications in the cell cycle regulation.
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