Contact: Caroline Perry
Caption: The Harvard researchers proposed a mechanism to explain how the stiffness and composition of the extracellular matrix could activate signaling pathways that produce a malignant phenotype. In normal conditions (left column), membrane components can fluctuate, overlap, and cluster, forming hemidesmosomes. In a stiffer matrix, they are unable to do so (center). The problem can be corrected in vitro by increasing the concentration of laminin (right).
Credit: Image courtesy of Ovijit Chaudhuri, Harvard University.
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