actin, motility and cancer

ScienceDirect – Seminars in Cancer Biology, Volume 18, Issue 1, Pages 1-76 (February 2008) has 8 reviews about actin, cytoskeleton, motility and cancer.

As written below:

Editorial: Actin is where it’s at

The development of malignant tumor cells is caused by changes in mechanisms altering the social behavior of cells in the organism, i.e. increased rate of proliferation, appearance of mechanisms allowing cells to escape from the confines of organ and vessel barriers, and increased motile activity/migration. The realization that growth factor receptors are directly involved in controlling not only proliferation but also cell motility and migration, and that alterations in the actin microfilament (MF)-system, the component behind motility/migration, are crucial to the development of malignancy, has led to intensive research efforts aiming at a complete elucidation of the physiology of the MF-system. The MF-system exists in all eukaryotic cells as part of the barrier between the cell interior and the outside world. It generates force for various kinds of translocations, involving whole cells or intracellular structures. Although there has been great progress in our understanding of the physiological importance of the MF-system, many aspects of actin microfilament formation and its regulation are still unclear.

In a seminal paper “Modelling the molecular circuitry of cancer” published in Cell (2000), Hanahan and Weinberg described signal transduction mechanisms, which are altered in malignant cells and how cancerogenesis is caused by accumulation of genetic alterations, releasing cells from the homeostatic mechanisms controlling normal proliferation.

The point made in the series of papers presented in this issue of SCB is that the alterations in signal transduction processes seen in the development of malignant cells, all, in one way or another, affect the control and/or functioning of the MF-system. Of particular interest is the close relationship that exists between the turnover in the phosphatidyl inositol cycle and the cell motility cycle, where the PI3 kinase, the production of PI4,5P2, PI3,4,5P3, and the PTEN protein (phosphatase homologous to tensin) are important regulatory components. As the story has unraveled, actin filament formation, cell adhesion mechanisms (integrins and cadherins), and signaling between the cell surface and the nucleus has become more and more interesting in relation to the appearance of malignant cancer cells.

It is our hope that this issue of SCB will stimulate further studies of the molecular mechanisms behind force generation and the development of the malignant state.