Abstract

Clusterin: Its Relevance to Antitumour Drug Sensitivity

Maximino Redondo

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 [1]. 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.