Inhibition of cell migration and invasion mediated by the TAT-RasGAP317-326 peptide requires the DLC1 tumor suppressor.

Abstract	TAT-RasGAP(317-326), a peptide corresponding to the 317-326 sequence of p120 RasGAP coupled with a cell-permeable TAT-derived peptide, sensitizes the death response of various tumor cells to several anticancer treatments. We now report that this peptide is also able to increase cell adherence, prevent cell migration and inhibit matrix invasion. This is accompanied by a marked modification of the actin cytoskeleton and focal adhesion redistribution. Interestingly, integrins and the small Rho GTP-binding protein, which are well-characterized proteins modulating actin fibers, adhesion and migration, do not appear to be required for the pro-adhesive properties of TAT-RasGAP(317-326). In contrast, deleted in liver cancer-1, a tumor suppressor protein, the expression of which is often deregulated in cancer cells, was found to be required for TAT-RasGAP(317-326) to promote cell adherence and inhibit migration. These results show that TAT-RasGAP(317-326), besides its ability to favor tumor cell death, hampers cell migration and invasion.
Authors	D Barras, G Lorusso, C Rüegg, C Widmann
Journal	Oncogene (Oncogene) Vol. 33 Issue 44 Pg. 5163-72 (Oct 30 2014) ISSN: 1476-5594 [Electronic] England
PMID	24213569 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Actins DLC-1 (deleted in liver cancer) protein, mouse DLC1 protein, human GTPase-Activating Proteins Hyaluronan Receptors Integrins Peptide Fragments TAT-RasGAP(317-326) Tumor Suppressor Proteins rho-Associated Kinases
Topics	Actins (metabolism) Animals Cell Adhesion (drug effects) Cell Line, Tumor (drug effects) Cell Movement (drug effects, genetics) Fibroblasts GTPase-Activating Proteins (genetics, metabolism, pharmacology) Humans Hyaluronan Receptors (metabolism) Integrins (metabolism) Mice Peptide Fragments (pharmacology) Protein Processing, Post-Translational Tumor Suppressor Proteins (genetics, metabolism) rho-Associated Kinases (metabolism)

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