Sunitinib malate inhibits hemangioma cell growth and migration by suppressing focal adhesion kinase signaling
作者： Wihan Scholtz , Peace Mabeta
关键词:
摘要: Sunitinib malate is a small molecule that targets multiple receptor tyrosine kinases and blocks their activity. Receptors targeted by sunitinib are implicated in tumor vascularization overexpressed vascular tumors encountered infants, namely, hemangiomas. Of note there still no definitive treatment for these commonly occurring of infancy. The purpose this study was to investigate the effects on hemangioma using endothelial cells isolated from murine model neoplasm (sEnd.2). drug cell growth were evaluated crystal violet assay flow cytometry, while scratch employed measure migration. Proteins associated with migration angiogenesis detected western blotting. investigated further determine its production reactive oxygen species, parameter promotion neovascularization tumors. results showed significantly reduced sEnd.2 causing accumulate sub-G1 phase cycle, also induced significant decrease (P < 0.05). blot expression adhesion proteins, focal kinase paxillin at IC50 doses, although cadherin did not change In addition, transforming factor-β1 (TGF-β1) decreased sunitinib-treated same dose. proteins as well TGF-β1 regulate movement have been progression. Thus, may potential
sci-hub.st 参考文章(43)
Jayapal John Joseph, D. Sangeetha, Thandapani Gomathi, Sunitinib loaded chitosan nanoparticles formulation and its evaluation International Journal of Biological Macromolecules. ,vol. 82, pp. 952- 958 ,(2016) , 10.1016/J.IJBIOMAC.2015.10.079
L. León-Mateos, J. Mosquera, L. Antón Aparicio, Treatment of sunitinib-induced hypertension in solid tumor by nitric oxide donors☆ Redox biology. ,vol. 6, pp. 421- 425 ,(2015) , 10.1016/J.REDOX.2015.09.007
Yvette Drabsch, Peter ten Dijke, TGF-β signalling and its role in cancer progression and metastasis Cancer and Metastasis Reviews. ,vol. 31, pp. 553- 568 ,(2012) , 10.1007/S10555-012-9375-7
Peace Mabeta, Michael S. Pepper, Hemangiomas - current therapeutic strategies. The International Journal of Developmental Biology. ,vol. 55, pp. 431- 437 ,(2011) , 10.1387/IJDB.103221PM
L J Ignarro, R E Byrns, G M Buga, K S Wood, Endothelium-derived relaxing factor from pulmonary artery and vein possesses pharmacologic and chemical properties identical to those of nitric oxide radical. Circulation Research. ,vol. 61, pp. 866- 879 ,(1987) , 10.1161/01.RES.61.6.866
Sara M Weis, David A Cheresh, Tumor angiogenesis: molecular pathways and therapeutic targets Nature Medicine. ,vol. 17, pp. 1359- 1370 ,(2011) , 10.1038/NM.2537
Rakesh K Jain, Dan G Duda, Jeffrey W Clark, Jay S Loeffler, Lessons from phase III clinical trials on anti-VEGF therapy for cancer Nature Reviews Clinical Oncology. ,vol. 3, pp. 24- 40 ,(2006) , 10.1038/NCPONC0403
David Padua, Joan Massagué, Roles of TGFβ in metastasis Cell Research. ,vol. 19, pp. 89- 102 ,(2009) , 10.1038/CR.2008.316
Peace Mabeta, Michael S. Pepper, Inhibition of hemangioma development in a syngeneic mouse model correlates with bcl-2 suppression and the inhibition of Akt kinase activity Angiogenesis. ,vol. 15, pp. 131- 139 ,(2012) , 10.1007/S10456-011-9248-7
Vladimir Kirkin, Ralph Mazitschek, Jaya Krishnan, Anja Steffen, Johannes Waltenberger, Michael S. Pepper, Athanassios Giannis, Jonathan P. Sleeman, Characterization of indolinones which preferentially inhibit VEGF‐C‐ and VEGF‐D‐induced activation of VEGFR‐3 rather than VEGFR‐2 FEBS Journal. ,vol. 268, pp. 5530- 5540 ,(2001) , 10.1046/J.1432-1033.2001.02476.X