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000130329 1001_ $$0P:(DE-He78)830be4979a39935ac6272eaebad5982a$$aPhillips, Emma$$b0$$eFirst author$$udkfz
000130329 245__ $$aTargeting atypical protein kinase C iota reduces viability in glioblastoma stem-like cells via a notch signaling mechanism.
000130329 260__ $$aBognor Regis$$bWiley-Liss$$c2016
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000130329 520__ $$aIn a previous study, Protein Kinase C iota (PRKCI) emerged as an important candidate gene for glioblastoma (GBM) stem-like cell (GSC) survival. Here, we show that PKCι is overexpressed and activated in patient derived GSCs compared with normal neural stem cells and normal brain lysate, and that silencing of PRKCI in GSCs causes apoptosis, along with loss of clonogenicity and reduced proliferation. Notably, PRKCI silencing reduces tumor growth in vivo in a xenograft mouse model. PKCι has been intensively studied as a therapeutic target in non-small cell lung cancer, resulting in the identification of an inhibitor, aurothiomalate (ATM), which disrupts the PKCι/ERK signaling axis. However, we show that, although sensitive to pharmacological inhibition via a pseudosubstrate peptide inhibitor, GSCs are much less sensitive to ATM, suggesting that PKCι acts along a different signaling axis in GSCs. Gene expression profiling of PRKCI-silenced GSCs revealed a novel role of the Notch signaling pathway in PKCι mediated GSC survival. A proximity ligation assay showed that Notch1 and PKCι are in close proximity in GSCs. Targeting PKCι in the context of Notch signaling could be an effective way of attacking the GSC population in GBM.
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000130329 650_7 $$2NLM Chemicals$$aIsoenzymes
000130329 650_7 $$2NLM Chemicals$$aProtein Kinase Inhibitors
000130329 650_7 $$2NLM Chemicals$$aReceptors, Notch
000130329 650_7 $$0EC 2.7.11.13$$2NLM Chemicals$$aProtein Kinase C
000130329 650_7 $$0EC 2.7.11.13$$2NLM Chemicals$$aprotein kinase C lambda
000130329 7001_ $$0P:(DE-He78)929b2109a63146eb30e74f712ad74596$$aLang, Verena$$b1$$udkfz
000130329 7001_ $$0P:(DE-He78)4ee529c1a2fbd7e1328b7b0c6ac84910$$aBohlen, Jonathan$$b2$$udkfz
000130329 7001_ $$0P:(DE-He78)06d81b4a485d027b97543964b7035573$$aBethke, Frederic$$b3$$udkfz
000130329 7001_ $$0P:(DE-He78)39a8becd6fa9602e4871d18f3f6f8e09$$aPuccio, Laura$$b4$$udkfz
000130329 7001_ $$0P:(DE-He78)2ef631585610340ff425c9c31fcabd03$$aTichy, Diana$$b5$$udkfz
000130329 7001_ $$0P:(DE-He78)c146c0b611b8fb654444ec078766f5ea$$aHerold-Mende, Christel$$b6$$udkfz
000130329 7001_ $$0P:(DE-He78)743a4a82daab55306a2c88b9f6bf8c2f$$aHielscher, Thomas$$b7$$udkfz
000130329 7001_ $$0P:(DE-He78)e13b4363c5fe858044ef8a39c02c870c$$aLichter, Peter$$b8$$udkfz
000130329 7001_ $$0P:(DE-HGF)0$$aGoidts, Violaine$$b9$$eLast author
000130329 773__ $$0PERI:(DE-600)1474822-8$$a10.1002/ijc.30234$$gVol. 139, no. 8, p. 1776 - 1787$$n8$$p1776 - 1787$$tInternational journal of cancer$$v139$$x0020-7136$$y2016
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