The Role of PTEN in Epithelial–Mesenchymal Transition

SIMPLE SUMMARY: The PTEN phosphatase is a ubiquitously expressed tumor suppressor, which inhibits the PI3K/AKT pathway in the cell. The PI3K/AKT pathway is considered to be one of the main signaling pathways that drives the proliferation of cancer cells. Furthermore, the same pathway controls the epithelial–mesenchymal transition (EMT). EMT is an evolutionarily conserved developmental program, which, upon aberrant reactivation, is also involved in the formation of cancer metastases. Importantly, metastasis is the leading cause of cancer-associated deaths. In this review, we discuss the literature data that highlight the role of PTEN in EMT. Based on this knowledge, we speculate about new possible strategies for cancer treatment. ABSTRACT: Phosphatase and Tensin Homolog deleted on Chromosome 10 (PTEN) is one of the critical tumor suppressor genes and the main negative regulator of the PI3K pathway. PTEN is frequently found to be inactivated, either partially or fully, in various malignancies. The PI3K/AKT pathway is considered to be one of the main signaling cues that drives the proliferation of cells. Perhaps it is not surprising, then, that this pathway is hyperactivated in highly proliferative tumors. Importantly, the PI3K/AKT pathway also coordinates the epithelial–mesenchymal transition (EMT), which is pivotal for the initiation of metastases and hence is regarded as an attractive target for the treatment of metastatic cancer. It was shown that PTEN suppresses EMT, although the exact mechanism of this effect is still not fully understood. This review is an attempt to systematize the published information on the role of PTEN in the development of malignant tumors, with a main focus on the regulation of the PI3K/AKT pathway in EMT.