Autocrine PF-02341066 cell line VEGF inhibition using a VEGF trap strongly increased in interphase microtubule dynamic instability (+ 43%). Consistently, exogenously added VEGF (10 ng/ml) suppressed microtubule dynamic instability (− 29%). Interestingly, the suppression of microtubule dynamics occurred through their plus end stabilisation at paxillin-containing focal adhesions. Moreover, VEGF increased EB1 comet length at microtubule plus end by 32 %, without any change in its expression level. Differential post-translational modifications of EB1 were detected by 2D electrophoresis and western blotting. Their characterizations are under investigation

by mass spectrometry. In conclusion, our results show (i) that microtubules integrate signals from the tumor microenvironment, (ii) that VEGF and MTA have opposite effect on microtubule and EB1 dynamics

supporting the clinical benefit of the therapeutic combination of VEGF inhibitors and MTA, and (iii) suggest a potential role of EB1 SYN-117 concentration protein in angiogenesis. 1- Pasquier E, et al Cancer Res 2005. 2- Pourroy B, et al Cancer Res 2006. 3- Honoré S, et al JPH203 in vitro Mol Cancer Ther.2008. Poster No. 193 3D Models to Track Endothelial Progenitors to a Tumor Site Application to In Vivo Imaging of Cell Migration Krzysztof Szade1,2, Witold Nowak1,2, Catherine Grillon1, Nathalie Lamerant-Fayel1, Alan Guichard1, David Gosset1, Alicja Jozkowicz2, Jozef Dulak2, Claudine Kieda 1 1 Centre de Biophysique Moléculaire, UPR 4301, CNRS, Orléans, France, 2 Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics

and Biotechnology, Kraków, Poland Tumor angiogenesis is crucial to support tumor cells growth and allow them to form metastasis [1]. Endothelial progenitor cells (EPC) are key players that influence tumor neovascularisation being directly incorporated into the tumor vessels [2]. Subsequently, we use progenitors of endothelium as vehicles for killer genes to be expressed preferentially in tumors [3]. This needs to determine the chemokines network that guides the progenitor and stem cells toward tumor. Here, we study mice model of melonama (B16F10 cells) and primitive endothelial precursors however isolated from mice embryo (MAgEC – Murine Aorta-gonad-mesonephros Endothelial Cells). To investigate the potential of B16F10 cells to stimulate MAgECs migration we applied two in-vitro methods with usage of fluorescence and pseudo confocal video microscopy, applied to dynamic phenomena using shear stress conditions and time lapse measurements on long term experiments. The first method was based on transwell inserts and visualization of MAgEC invasion through Matrigel. In the second one, 3D tumor spheroids were formed and migration of MAgEC through collagen gel towards spheroids was investigated. This allows to study the chemokine activity as we showed that CCL21 augments MAgEC sensitivity and migration potential. Such “education” may be important in cell based therapy against tumor.