Article Text

other Versions

PDF
Molecular interactions of polo-like kinase 1 in human cancers
  1. Wayne Tiong Weng Ng1,2,3,
  2. Joo-Shik Shin1,2,3,4,5,
  3. Tara Laurine Roberts2,4,
  4. Bin Wang1,2,6,
  5. Cheok Soon Lee1,2,3,4,5,6,7
  1. 1Discipline of Pathology, School of Medicine, Western Sydney University, Sydney, Australia
  2. 2Centre for Oncology Education and Research Translation (CONCERT), Ingham Institute for Applied Medical Research, Sydney, Australia
  3. 3Cancer Pathology and Cell Biology Laboratory, Ingham Institute for Applied Medical Research, Sydney, Australia
  4. 4Molecular Medicine Research Group, School of Medicine, Western Sydney University, Sydney, Australia
  5. 5Department of Anatomical Pathology, Liverpool Hospital, Sydney, Australia
  6. 6South Western Sydney Clinical School, University of New South Wales, Sydney, Australia
  7. 7Cancer Pathology, Bosch Institute, University of Sydney, Sydney, Australia
  1. Correspondence to Wayne Ng, Centre for Oncology Education and Research Translation (CONCERT), Ingham Institute for Applied Medical Research, 1 Campbell St, Liverpool NSW 2170, Australia; W.Ng{at}westernsydney.edu.au; soon.lee{at}westernsydney.edu.au

Abstract

Polo-like kinase 1 (PLK1) is an essential protein in communicating cell-cycle progression and DNA damage. Overexpression of PLK1 has been validated as a marker for poor prognosis in many cancers. PLK1 knockdown decreases the survival of cancer cells. PLK1 is therefore an attractive target for anticancer treatments. Several inhibitors have been developed, and some have been clinically tested to show additive effects with conventional therapies. Upstream regulation of PLK1 involves multiple interactions of proteins such as FoxM1, E2F and p21. Other cancer-related proteins such as pRB and p53 also indirectly influence PLK1 expression. With the high mutation rates of these genes seen in cancers, they may be associated with PLK1 deregulation. This raises the question of whether PLK1 overexpression is a cause or a consequence of oncogenesis. In addition, hypomethylation of the CpG island of the PLK1 promoter region contributes to its upregulation. PLK1 expression can be affected by many factors; thus, it is possible that PLK1 deregulation in each individual patient tumours could be due to different underlying mechanisms.

  • CANCER
  • MOLECULAR PATHOLOGY
  • TUMOUR MARKERS
  • CELL CYCLE REGULATION

Statistics from Altmetric.com

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.