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The cadherin switch is also essential for increased motility, but is not always required for the morphological changes that accompany EMT (Maeda et al, 2005).
These figures indicate a general trend for increased motility in the SI populations vs NI or I, with the exception of the MDA-MB-435S-F/Taxol-10p4p SI population.
Matrix modification is a well-established requirement for increased motility of VSMC and other cell types.
The expression of FPR is responsible for increased motility of human glioblastoma cells and their formation of highly invasive tumours.
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That is, no amount of increased motility can compensate for too low a growth rate.
One mechanism for this increased motility is the activation of plasmin by extracellular hsp90α.
Tyrosine phosphorylation of EMS1/cortactin is required for the increased motility of cells engineered to overexpress this protein [ 35*].
These mutations also resulted in constitutive tyrosine phosphorylation on several cellular proteins including paxillin at key tyrosine residues and may account for the increased motility of cells with this mutation.
To investigate if this system could be responsible for the increased motility observed in cells with TFPI downregulated, the plasmin activator, uPA, and its inhibitor, PAI-1, were analyzed.
These results indicate the presence of FPR agonists in FCS and HS and provide a basis for the increased motility of FPR+ tumour cells in the absence of the defined FPR agonists fMLF.
As mentioned before, a tumor is a complex, dynamic system where cells compete for resources, and while increased motility should actually be disadvantageous in a homogeneous environment, increased mobility can be advantageous under variably harsh conditions (Chen et al. 2011).
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