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For example, cortex contractility plays a crucial role in amoeboid migration of metastatic cells [6] and during division, where its misregulation can lead to aneuploidy [7].
EP receptor antagonists SC-19220, AH-6809, and AH-23848B, having highest affinity for EP1, EP1/EP2/DP, and EP4 receptors, respectively, variably inhibited migration of metastatic breast cancer cells.
These collagen fibers are highly aligned and well organized to provide preferential, enhanced migration of metastatic tumor cells [ 25, 31].
Exercise also seemed to stabilize the tumor vascular system, leading to an improved endothelial barrier which may constrict the migration of metastatic cells.
For example, cortex contractility plays a crucial role in amoeboid migration of metastatic cells [ 6] and during division, where its misregulation can lead to aneuploidy [ 7].
Moreover, the migration of metastatic breast cancer cells can be increased by the interaction of CD44v3, 8 to 10 with ankyrin promoted by Rho kinase [ 31].
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To address this question, we performed transwell migration assays which confirmed that IL13Rα2 depletion accompanied by IL-13 treatment could additively reduce the migration rate of metastatic MIV cells (Fig. 5d and Additional file 7: Figure S6).
Furthermore, compounds 3b and 11b inhibit migration activity of metastatic cell line MDA-MB-231 by 32%and34%4%, respectively.
The effect of PRDX3 siRNA transient transfection on migration capability of metastatic 5-8F cells was showed.
To determine a role for Cdc42 in the migration of highly metastatic cells, we expressed vector alone and a dominant negative myc-tagged Cdc42(T17N) construct in the highly metastatic MDA-MB-435α6HG6 cell variant and subjected both to a migration assay.
Moreover, sipholanes showed promising in vitro inhibitory effects against the invasion and migration of the metastatic human breast cancer cell line MDA-MB-231.
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