FASEB J.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by AHMAD, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by AHMAD, N.
(The FASEB Journal. 2004;18:5-7.)
© 2004 FASEB

Polo-like kinase (Plk) 1: a novel target for the treatment of prostate cancer

NIHAL AHMAD1

Department of Dermatology, University of Wisconsin Comprehensive Cancer Center, Molecular and Environmental Toxicology Center, University of Wisconsin, Madison, Wisconsin, USA

1Correspondence: Department of Dermatology, University of Wisconsin, Medical Science Center, 1300 University Ave., Madison, WI 53706, USA. E-mail: nahmad{at}wisc.edu

ABSTRACT

Second only to skin cancer, cancer of the prostate gland (CaP) is the most commonly occurring cancer in American men. Existing treatment approaches and surgical intervention have been unable to effectively manage this dreaded cancer; therefore, efforts are ongoing to explore novel targets and strategies for the management of CaP. A complete understanding of the genetic control of the processes of cellular proliferation and programmed cell death, or "apoptosis," may provide the basis for the rational design of novel therapeutic strategies against CaP. Key regulators for the mitotic progression in mammalian cells are the polo-like kinases (Plks). The activity of Plk1 is elevated in tissues and cells with a high mitotic index, including cancer cells. An increasing body of evidence suggests that the level of Plk1 expression has prognostic value for predicting outcomes in patients with some cancers such as lung cancer, squamous cell carcinomas of the head and neck, melanomas, and ovarian and endometrial carcinomas. However, the role of Plk1 in CaP is not known. Here, a hypothesis is put forward that Plk 1 plays a critical role in the development of prostate cancer; and the silencing of Plk1 will result in elimination of human CaP cells via an inactivation of cyclin-dependent kinase 1 (Cdc2)/cyclin B 1-mediated mitotic arrest followed by apoptosis. A corollary to this hypothesis is that Plk1 could serve as a target for the intervention of CaP in humans. Therefore, if the hypothesis is tested to be true, it is conceivable that gene therapeutic approaches aimed at Plk1 or the pharmacological inhibitors of Plk1 may be developed for the treatment/management of CaP.—Ahmad, N. Polo-like kinase (Plk) 1: a novel target for the treatment of prostate cancer.


Key Words: Plk inhibitor • gene therapy • apoptosis • cell cycle




This article has been cited by other articles:


Home page
Clin. Cancer Res.Home page
L. L. Garland, C. Taylor, D. L. Pilkington, J. L. Cohen, and D. D. Von Hoff
A Phase I Pharmacokinetic Study of HMN-214, a Novel Oral Stilbene Derivative with Polo-Like Kinase-1-Interacting Properties, in Patients with Advanced Solid Tumors
Clin. Cancer Res., September 1, 2006; 12(17): 5182 - 5189.
[Abstract] [Full Text] [PDF]


Home page
Cancer Res.Home page
B. Spankuch, S. Heim, E. Kurunci-Csacsko, C. Lindenau, J. Yuan, M. Kaufmann, and K. Strebhardt
Down-regulation of Polo-like Kinase 1 Elevates Drug Sensitivity of Breast Cancer Cells In vitro and In vivo
Cancer Res., June 1, 2006; 66(11): 5836 - 5846.
[Abstract] [Full Text] [PDF]


Home page
Hum Mol GenetHome page
A. Astrinidis, W. Senapedis, and E. P. Henske
Hamartin, the tuberous sclerosis complex 1 gene product, interacts with polo-like kinase 1 in a phosphorylation-dependent manner
Hum. Mol. Genet., January 15, 2006; 15(2): 287 - 297.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2004 by The Federation of American Societies for Experimental Biology.