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Abstract
Decades of research have shown that there is an intimate relationship between the extracellular matrix (ECM) and cellular phenotype. While the existence of this relationship remains inarguably clear, the exact details through which the extracellular matrix controls phenotypic behavior at the gene expression level are, for the most part, elusive. In a recent study on mammary epithelial cells, nuclear actin was identified as a key effector protein through which laminin type III (LN1) attenuates RNA polymerase activity to promote growth arrest. This finding forms the basis from which one can begin to envision a mechanism through which the ECM can control nuclear function to enact changes in cell behavior. Here I will briefly discuss the current depth of knowledge with regards to the relationship between LN1 and nuclear actin and its implication in mammary epithelial cell growth and function.
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