Clusterin: Its Relevance to Antitumour Drug SensitivityMaximino Redondo*
Department of Biochemistry, Hospital Costa del Sol, University of Málaga, CIBER ESP, Spain
- *Corresponding Author:
- Dr. Maximino Redondo
Department of Biochemistry
Hospital Costa del Sol
University of Málaga
CIBER ESP, Carretera de Cádiz km 187
29600, Marbella, Málaga, Spain
E-mail: [email protected]
Received Date: September 08, 2011; Accepted Date: September 10, 2011; Published Date: November 12, 2011
Citation: Redondo M (2011) Clusterin: Its Relevance to Antitumour Drug Sensitivity. Clinic Experiment Pharmacol 1:e101. doi: 10.4172/2161-1459.1000e101
Copyright: © 2011 Redondo M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Chemotherapy resistance is a major problem in disease management and the principal factor underlying most cancer deaths. Therefore, a primary goal in cancer research is to develop new ways of inhibiting cancer growth, in part by improving the effectiveness of existing cancer regimens. Resistance to cancer treatment is known to be mediated, at least in part, by the enhanced expression of cell survival proteins that facilitate tumour progression. In this respect, the clusterin protein (CLU) has drawn much attention because of its association with tumorigenesis and progression and its implication in two contrasting functions, survival and apoptosis, which are carry out by two different forms (secretory, s-CLU and nuclear, n-CLU, respectively). Most authors agree that tumour cell survival is related to the overexpression of sCLU and the loss of n-CLU . It is noteworthy that only the cytoplasmic /secretory CLU form (sCLU) and not the nuclear form (nCLU) is expressed in aggressive late stage tumours, which is in line with its anti-apoptotic function. At present, there is no doubt as to the dual forms and functions of CLU.