Crosstalk Between Plk1 and PTEN in Mitosis Affects Chromosomal Stability.

Abstract

The mitotic phase involves the distribution and regulation of genetic material. Defects in gene regulation can lead to serious errors in genetic transmission, such as increased instability of chromosomes, thereby increasing susceptibility to cancer and promoting its development. The maintenance of chromosome stability depends on several mechanisms, such as efficient DNA repair, proper sister chromatid separation, and timely cytokinesis. The serine/threonine kinase Plk1 is a key molecule in maintaining chromosome stability, participating in multiple stages of precise regulation during mitosis, including promoting entry into mitosis, facilitating centrosome maturation and bipolar spindle formation, promoting sister chromatid separation, and facilitating cytokinesis. Several proteins can regulate the kinase activity of Plk1 through protein-protein interactions, coordinating the genetic stability of the cell, including the kinases Aurora A, c-Abl, and Chk1 as well as the phosphatase phosphatase and tension homolog (PTEN). PTEN has been described as an essential regulator of Plk1 for dephosphorylation and chromosomal stability during cell division, and Plk1 may directly interact with and phosphorylate PTEN at centromeres. Here, we review the bidirectional interplay between Plk1 and PTEN and how it contributes to genomic stability during mitosis.