Abstract
PTEN is a tumor suppressor gene inactivated in various human cancers, which antagonizes PI3K activity. The PI3K/AKT pathway is frequently activated in cancer, then, the PTEN tumor suppressor may be the major brake of the pathway. Cells that lack functional PTEN gene have constitutively higher levels of PIP3 and activated downstream targets. The PTEN protein binds to the MAGI proteins (MAGIs), which are scaffolding molecules with PDZ domain involved in the regulation of epithelial cell tight-junction assembly. Studies have revealed the potential relevance of the PDZ interactions to cancer cell behaviors. The molecular mechanisms contributing to cancer invasion are the subject of considerable investigation, as a better understanding of the pathogenesis will lead to the development of novel targeted therapies. We review recent studies on the features of PTEN and MAGIs in the signaling pathways involved in cancer progression.
Highlights
The PI3K/AKT pathway has been shown to play a pivotal role on the initiation and progression of malignancies, enhancing cell survival by stimulating cell proliferation, and inhibiting apoptosis [1,2] (Figure 1)
The PTEN interacts with PDZ domain-containing molecules including MAGI proteins (MAGIs), which are scaffolding molecules involved in the regulation of tight-junction assembly and are involved in diverse regulatory pathways including the control of cell-attachment [6]
The PTEN tumor suppressor is recruited to E-cadherin junctional complexes through the binding to the second PDZ domain of the MAGI-1b [11]
Summary
The PI3K/AKT pathway has been shown to play a pivotal role on the initiation and progression of malignancies, enhancing cell survival by stimulating cell proliferation, and inhibiting apoptosis [1,2] (Figure 1). PTEN plays a critical role in MAGIs-induced inhibition of cell migration and proliferation in cancers. The PTEN tumor suppressor is recruited to E-cadherin junctional complexes through the binding to the second PDZ domain of the MAGI-1b [11].
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