Polo-like kinase (Plk) 1 as a target for prostate cancer management

Shannon Reagan-Shaw1, Nihal Ahmad

  • 1Department of Dermatology, University of Wisconsin, Madison, Wisconsin, USA.

IUBMB Life
|October 15, 2005
PubMed

Insights

Polo-like kinase 1 (Plk1) is overexpressed in prostate cancer, indicating its potential as a therapeutic target. Targeting Plk1 may offer new strategies for prostate cancer treatment and prevention.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Prostate cancer (PCa) is a leading cancer in American men, with current treatments often proving insufficient.
  • Novel therapeutic targets and strategies are crucial for effective PCa management.
  • The serine/threonine kinase Polo-like kinase (Plk) 1 is implicated in cell proliferation and mitosis.

Purpose of the Study:

  • To review the role of Polo-like kinase (Plk) 1 in prostate cancer.
  • To evaluate Plk1 as a potential therapeutic target for prostate cancer treatment and chemoprevention.

Main Methods:

  • Literature review of studies investigating Plk1 expression and function in prostate cancer.
  • Analysis of Plk1's role in cell cycle regulation and mitosis.
  • Examination of Plk1 as a prognostic indicator in various tumor types.

Main Results:

  • Plk1 is overexpressed in numerous cancer types, including prostate cancer.
  • Aberrant Plk1 elevation is frequently associated with poor prognosis.
  • Plk1 regulates key mitotic events essential for cell division and cytokinesis.

Conclusions:

  • Polo-like kinase (Plk) 1 is a promising target for novel prostate cancer therapies.
  • Targeting Plk1 could be beneficial for both treatment and chemoprevention of prostate cancer.

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Protein Kinases and Phosphatases02:54

Protein Kinases and Phosphatases

Proteins undergo chemical modifications that trigger changes in the charge, structure, and conformation of the proteins. Phosphorylation, acetylation, glycosylation, nitrosylation, ubiquitination, lipidation, methylation, and proteolysis are various protein modifications that regulate protein activity. Such modifications are usually enzyme-driven.
Protein kinases
Many proteins in the cell are regulated by phosphorylation, the addition of a phosphate group. A family of enzymes called kinases...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...