Stathmin in Cell Proliferation and Cancer Progression

The phosphoprotein stathmin exerts profound influences on cell proliferation, differentiation and in cell motility. These phenotypic features are displayed in response to specific signals imparted to the cell by biological response modifiers. Stathmin functions as a focal point in co-ordinating and directing the cellular signals into specific and defined pathways. Two biological features that characterise cancer are the deregulation of cell proliferation leading to tumour growth and invasive behaviour. Stathmin is up-regulated in many neoplasms and the modulation of its expression correlates with invasion and metastasis and highly proliferating normal tissues. The integrity of the transduction of extracellular signals is essential for the normal functioning of the cellular machinery in cell differentiation, morphogenesis and cell proliferation, apoptosis, growth and senescence. Stathmin mediates these pathways of signalling. Stathmin has been implicated in both G₁-S and G₂-M checkpoint control of cell cycle progression by influencing the dynamics of microtubule formation and progression of the cell cycle. Stathmin appears to exert its regulatory effects at both G₁-S and G₂-M checkpoints by interacting with other cell cycle control proteins such as p53 and rb and with cancer metastasis promoting or inhibiting genes as well as other proteins such as heat shock proteins. Stathmin co-ordinates the signalling by extracellular matrix proteins, and defines intercellular adhesion and cell motility. Therefore, the deregulation of stathmin function would have profound implications in the pathogenesis and progression of cancer.