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PLK1 Induces Chromosomal Instability and Overrides Cell-Cycle Checkpoints to Drive Tumorigenesis. | LitMetric

PLK1 Induces Chromosomal Instability and Overrides Cell-Cycle Checkpoints to Drive Tumorigenesis.

Cancer Res

Department of Human and Molecular Genetics, VCU Institute of Molecular Medicine, VCU Massey Cancer Center, Virginia Commonwealth University, School of Medicine, Richmond, Virginia.

Published: March 2021

AI Article Synopsis

  • * Transgenic mice engineered to have high PLK1 levels developed multiple types of spontaneous tumors, showing that excessive PLK1 can disrupt normal cell division and lead to chromosomal instability (CIN).
  • * The study suggests that high PLK1 expression correlates with genomic alterations in human cancers, indicating its potential as a target for cancer therapies aimed at tumors with CIN.

Article Abstract

Polo-like kinase 1 (PLK1) is an essential cell-cycle regulator that is frequently overexpressed in various human cancers. To determine whether Plk1 overexpression drives tumorigenesis, we established transgenic mouse lines that ubiquitously express increased levels of Plk1. High Plk1 levels were a driving force for different types of spontaneous tumors. Increased Plk1 levels resulted in multiple defects in mitosis and cytokinesis, supernumerary centrosomes, and compromised cell-cycle checkpoints, allowing accumulation of chromosomal instability (CIN), which resulted in aneuploidy and tumor formation. Clinically, higher expression of PLK1 positively associated with an increase in genome-wide copy-number alterations in multiple human cancers. This study provides evidence that aberrant expression of PLK1 triggers CIN and tumorigenesis and highlights potential therapeutic opportunities for CIN-positive cancers. SIGNIFICANCE: These findings establish roles for PLK1 as a potent proto-oncogene and a CIN gene and provide insights for the development of effective treatment regimens across PLK1-overexpressing and CIN-positive cancers.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8026515PMC
http://dx.doi.org/10.1158/0008-5472.CAN-20-1377DOI Listing

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