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. 2011 Aug 23;105(7):1002–1011. doi: 10.1038/bjc.2011.303

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Copyright © 2011 Cancer Research UK

This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/.

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The truncated form of CD9-P1, GS-168AT2, inhibits dose-dependently in vitro hEC proliferation and migration. (A) Schematic representation of the structure of CD9-P1, the cloned truncated CD9-P1 domain, GS-168AT2, and the produced Tag-recombinant protein. (B) SDS–PAGE imprints (lane 1, molecular mass marker; lane 2 purified GS-168AT2) and the corresponding WB (lane 3, using 229 mAb) of the purified GS-168AT2 used for the all subsequent experiments. (C) Dose-response curve of the effects of GS168AT2 on the proliferation of hEC. Results were expressed as percentage of control±s.e. (n=4). Statistical significance between the control and the different doses of GS-168AT2 were calculated with two-tailed Student's t-test (^*P<0.05; ^**P<0.01; ^***P<0.001). (D) Representative images at 18 h of the wounded hEC monolayer incubated with either vehicle or increasing concentrations of GS-168AT2.