Actin, its associated proteins and metastasis.

Abstract

In this short article we have overviewed the effect of transformation on AAPs. We have not dealt with molecules indirectly associated with actin which are modified by transformation, such as the catenins, cadherins, vinculin, and integrins [Tsukita et al., 1993], although their relationship with and importance to the transformed phenotype cannot be overemphasised. Similarly, alterations in polyphosphoinositide metabolism that occur in transformed cells may also promote or induce alterations in the microfilament cytoskeleton via interactions with proteins such as gelsolin, alpha-actinin, and MARCKS [Bretscher, 1993]. At present, there are no clear-cut rules regarding the effect that oncogenesis has on AAPs, since the expression level of one oncogenically modified AAP can vary from one tumour to another, even within the same type of tumour [Yamamoto et al., 1993]. This apparent inconsistency may well be because we are "playing with an incomplete pack of cards" [Pollard, 1993], or it may reflect this highly complex control mechanism in which any perturbation of the normal expression levels of actin/AAPs unbalances the delicate equilibrium which controls normal cell behaviour [Bray and Vasiliev, 1989]. For example, it is possible that oncogenically induced alterations to actin isoform expression [Lin et al., 1985] exert a downstream effect on actin-associated protein expression. Oncogenically induced actin based cell movements may be activated by alterations to either a single AAP or a synergistic functional unit of these molecules [Shapland et al., 1993; Vandekerckhove et al., 1990].(ABSTRACT TRUNCATED AT 250 WORDS)