000126144 001__ 126144
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000126144 0247_ $$2doi$$a10.18632/oncotarget.3369
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000126144 0247_ $$2pmc$$apmc:PMC4496193
000126144 037__ $$aDKFZ-2017-02259
000126144 041__ $$aeng
000126144 082__ $$a610
000126144 1001_ $$aBhatia, Shilpa$$b0
000126144 245__ $$aKnockdown of EphB1 receptor decreases medulloblastoma cell growth and migration and increases cellular radiosensitization.
000126144 260__ $$a[S.l.]$$bImpact Journals LLC$$c2015
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000126144 520__ $$aThe expression of members of the Eph family of receptor tyrosine kinases and their ephrin ligands is frequently dysregulated in medulloblastomas. We assessed the expression and functional role of EphB1 in medulloblastoma cell lines and engineered mouse models. mRNA and protein expression profiling showed expression of EphB1 receptor in the human medulloblastoma cell lines DAOY and UW228. EphB1 downregulation reduced cell growth and viability, decreased the expression of important cell cycle regulators, and increased the percentage of cells in G1 phase of the cell cycle. It also modulated the expression of proliferation, and cell survival markers. In addition, EphB1 knockdown in DAOY cells resulted in significant decrease in migration, which correlated with decreased β1-integrin expression and levels of phosphorylated Src. Furthermore, EphB1 knockdown enhanced cellular radiosensitization of medulloblastoma cells in culture and in a genetically engineered mouse medulloblastoma model. Using genetically engineered mouse models, we established that genetic loss of EphB1 resulted in a significant delay in tumor recurrence following irradiation compared to EphB1-expressing control tumors. Taken together, our findings establish that EphB1 plays a key role in medulloblastoma cell growth, viability, migration, and radiation sensitivity, making EphB1 a promising therapeutic target.
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000126144 650_7 $$2NLM Chemicals$$aAntigens, CD29
000126144 650_7 $$2NLM Chemicals$$aCell Cycle Proteins
000126144 650_7 $$2NLM Chemicals$$aNeoplasm Proteins
000126144 650_7 $$2NLM Chemicals$$aRNA, Small Interfering
000126144 650_7 $$0EC 2.7.10.1$$2NLM Chemicals$$aReceptor, EphB1
000126144 650_7 $$0EC 2.7.10.2$$2NLM Chemicals$$aProto-Oncogene Proteins pp60(c-src)
000126144 7001_ $$aBaig, Nimrah A$$b1
000126144 7001_ $$aTimofeeva, Olga$$b2
000126144 7001_ $$aPasquale, Elena B$$b3
000126144 7001_ $$aHirsch, Kellen$$b4
000126144 7001_ $$aMacDonald, Tobey J$$b5
000126144 7001_ $$aDritschilo, Anatoly$$b6
000126144 7001_ $$aLee, Yi Chien$$b7
000126144 7001_ $$aHenkemeyer, Mark$$b8
000126144 7001_ $$aRood, Brian$$b9
000126144 7001_ $$aJung, Mira$$b10
000126144 7001_ $$aWang, Xiao-Jing$$b11
000126144 7001_ $$0P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8$$aKool, Marcel$$b12$$udkfz
000126144 7001_ $$aRodriguez, Olga$$b13
000126144 7001_ $$aAlbanese, Chris$$b14
000126144 7001_ $$aKaram, Sana D$$b15
000126144 773__ $$0PERI:(DE-600)2560162-3$$a10.18632/oncotarget.3369$$gVol. 6, no. 11, p. 8929 - 8946$$n11$$p8929 - 8946$$tOncoTarget$$v6$$x1949-2553$$y2015
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000126144 9141_ $$y2015
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