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Cyclin D1 has previously been reported to regulate cellular migration in primary bone macrophages, mouse embryo fibroblasts (MEFs), and breast cancer cells [ 52- 54].
Tandutinib suppressed cell migration in primary meningiomas as effectively as sunitinib, in spite of the fact that tandutinib only inhibits PDGFR β.
These data suggest that a recapitulation of developmental programs may be adopted by the breast tumor cells and their partner macrophages during invasion and migration in primary tumors.
CadN mediated adhesive interactions were shown to be essential for growth cone migration in primary neuronal cultures (Bard et al., 2008).
These results confirmed that oscillations of Rac activity along the central longitudinal axis of the cell are a hallmark of directional migration in primary mouse neutrophils.
HIF-1 induction of LOX and LOXL-2 has been shown to promote migration in primary renal epithelial, and in breast and cervical cancer cells, which was associated with decreased E-cadherin expression [ 5, 25].
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We therefore set out to investigate the relative importance of PKD enzymes in regulating integrin-mediated cell adhesion and migration responses in primary lymphocytes.
We also predict that direct measures of cell migration in the primary tumor, perhaps through measures of genes expression and proteins in cell migration pathways, should be good biomarkers for the risk of metastasis.
Loss of these two IAPs stabilizes Rac1 and promotes an elongated-mesenchymal mode of migration in many primary and tumor cell lines (discussed below).
We report for the first time a gene-expression profile for human breast tumor cells specific to the processes of invasion and migration in the primary tumor.
In vitro migration was assessed in primary and normal synoviocytes (synovial fibroblast cells (SFCs)) using a wound repair scratch assay.
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