A protein called fascin play a critical transformation role in TGF beta mediated tumor metastasis, say researchers at Moffitt Cancer Center in Tampa, In a study pubblished in Journal of Biological Chemistry by Shengyu Yang, Ph.D, result that elevated Transforming Growth Factor beta in the tumor microenvironment may be responsible for fascin over-expression, which in turn can promote metastasis in some metastatic tumors. The researchers explained that fascin levels are low or not detected in normal tissues, but are highly elevated in malignant tumors. Also, high fascin expression is associated with poor prognosis. It has been clear for some time, they noted, that there is a causal role for fascin over-expression in tumor cell dissemination. However, the underlying mechanism for the elevation of fascin levels has not been clarified. Their analysis using cell culture- based assay and patient microarray data mining strongly suggests that elevated TGF beta levels in tumors lead to fascin overexpression, which in turn promotes metastasis. While there have been many studies on the role of fascin in tumor cell migration and metastasis, the current study is first to report that TGF beta elevates fascin protein expression to promote invasion, particularly in tumor cells of spindle-shaped – the kind of morphology associated with high tumor invasiveness and more metastatic disease. “The finding that TGF beta only induces fascin over-expression in highly metastatic tumor cells is especially interesting,” said Yang. “Therapies targeting fascin may block TGF beta mediated metastasis without interfering with the tumor suppressor role of TGF beta in normal tissues.”
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