RTK-induced SRC activation may also be responsible for the regulation of specific human tumor phenotypes such as cell invasion and motility, which can increase the metastatic potential of a tumor, as SRC targets substrates involved in the processes of cellular adhesion and migration [50].
Both, 0.2 ng/ml exogenous TGF-β and CoCM, were capable of inducing scattering of MCF-7 and T47D cells (Fig. S3), indicating that low concentrations of TGF-β as found in CoCM can increase motility of several breast cancer cell lines.
In support of this hypothesis, ligand-independent, constitutively active forms of EGFR can increase motility and invasiveness of tumor cells and EGFR inhibitors have been shown to inhibit cancer cell migration in vitro [ 62– 62].
In neutrophils, O-GlcNAcylation induced by GlcNH2 can increase cellular motility [12] and regulate activities of intermediates of Rac and PI3K involved in cellular migration [68].
Our previous study showed that angiopoietin-like 3 (Angptl3) can increase the motility of podocytes in vitro.
To summarize, our research provided an explanation for the phenomenon that Angptl3 can increase the motility of podocytes in vitro.
The following long-term lamellipodia formation caused by Rac1 stimulation can increase the motility of podocytes, which may aggravate foot process effacement and result in proteinuria.
The loss or presence of blood group antigens can increase cellular motility or facilitate the interaction between tumor cells and endothelial cells of distant organs [ 8– 11].
We have found that Angptl3 expression can increase podocytes motility [ 15], which suggests that Angptl3 may induce F-actin rearrangement in podocytes.
