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We then examined whether CXCL12 induced migration of primary cells was affected by TSAd expression using a transwell chemotaxis assay.
Further, our results with in vitro invasion assay using a transwell chemotaxis invasion approach in AsPC-1 and PANC-1 cells also showed that SMAD4 enhanced the invasive ability of PDAC cells in vitro (P < 0.05; Figure 2D and Additional file 1: Figure S1).
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We also examined the effect of SNAI2/Slug on chemotaxis in glioblastoma cells using a transwell migration assay and 10% serum as a chemoattractant.
Moreover, sFasL strongly inhibited VEGF165-induced chemotaxis of ECs, determined by using a Transwell chamber, whereas sCD40L (0.1 to 100 ng/ml) did not affect it.
To this aim, MSCs seeded in 3D scaffolds or 2D surfaces were co-cultured with macrophages using a transwell insert system and levels of soluble factors related with inflammation and chemotaxis were quantified.
To further verify that Notch signaling regulated macrophage infiltration through CCL2-CCR2 chemotaxis, we co-cultured RBP-J deficient or control macrophages with HEK293 cells overexpressing CCL2 using a transwell system.
The migration of cells was examined using a Transwell chamber.
We then assessed EPC migration using a transwell assay.
Cell migration was measured using a transwell chamber.
Migration activities of Treg subsets were assessed by using a transwell assay as previously described [26].
Migration of murine BMMCs was evaluated using a transwell migration assay [35].
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