Prostate cancer metastasis: Talking the walk. Coffey DS.
Nature Medicine 1996, 2:1305-1306. Thymosin b15: a novel regulator of tumor cell motility upregulated in prostate cancer.
Bao L, Loda M, Janmey PA, Stewart R, Anand-Apte B and Zetter BR
Nature Medicine 1996, 2:1322-1328.


The concept of cell walking is used by Coffey as an introduction to a paper from Boston on the subject of cell motility and its contribution to prostate cancer metastasis potential. Coffey discusses the loss of cell-cell adhesion (E-Cadherin/alpha-catenin/actin cytoskeleton), cell-basement membrane adhesion (integrin) following malignant transformation. Later still, extracellular proteolysis frees the tumour cells from their local constraints. Cell walking involves the formation of anterior adhesions with the release of posterior adhesions; it is a normal part of embryogenesis and is thought to be controlled by autocrine motility factors. A metastasis suppressor gene (KAI1) has been identified (chromosome 11p11.2) and Bao describes upregulation of Thymosin b15 (which sequesters G-actin) in prostate cancers of increasing Gleason grade while antisense constructs introduced to rat prostatic cancer cell lines caused reduced motility with unaltered cell proliferation.