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000181227 0247_ $$2doi$$a10.18632/oncotarget.22648
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000181227 037__ $$aDKFZ-2022-01875
000181227 041__ $$aEnglish
000181227 082__ $$a610
000181227 1001_ $$0P:(DE-He78)3caae9893e3b2704f7bb5a9646ef084d$$aJennemann, Richard$$b0$$eFirst author$$udkfz
000181227 245__ $$aInhibition of hepatocellular carcinoma growth by blockade of glycosphingolipid synthesis.
000181227 260__ $$a[S.l.]$$bImpact Journals LLC$$c2017
000181227 3367_ $$2DRIVER$$aarticle
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000181227 500__ $$aPOF Topic: 317
000181227 520__ $$aHepatocellular carcinoma (HCC) is one of the most frequent cancers. In vitro studies suggest that growth and response to therapy of human carcinomas may depend on glycosphingolipid (GSL) expression. Glucosylceramide synthase (GCS), encoded by the gene Ugcg, is the basic enzyme required for the synthesis of GSLs. Gene array analysis implied that Ugcg is significantly overexpressed in human HCC as compared to non-tumorous liver tissue. Therefore we have investigated whether tumor - genesis and - growth is altered in the absence of GSLs. An endogenous liver cancer model has been initiated by application of diethylnitrosamine in mice lacking Ugcg specifically in hepatocytes. We have now shown that hepatocellular tumor initiation and growth in mice is significantly inhibited by hepatic GSL deficiency in vivo. Neither the expression of cell cycle proteins, such as cyclins and pathways such as the MAP-kinase/Erk pathway nor the mTOR/Akt pathway as well as the number of liver infiltrating macrophages and T cells were essentially changed in tumors lacking GSLs. Significantly elevated bi-nucleation of atypical hepatocytes, a feature for impaired cytokinesis, was detected in tumors of mice lacking liver-specific GSLs. A reduction of proliferation and restricted growth of tumor microspheres due to delayed, GSL-dependent cytokinesis, analogous to the histopathologic phenotype in vivo could be demonstrated in vitro. GSL synthesis inhibition may thus constitute a potential therapeutic target for hepatocellular carcinoma.
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000181227 650_7 $$2Other$$acytokinesis
000181227 650_7 $$2Other$$aglycolipid
000181227 650_7 $$2Other$$aglycosphingolipid
000181227 650_7 $$2Other$$ahepatocellular carcinoma
000181227 650_7 $$2Other$$asphingomyelin
000181227 7001_ $$0P:(DE-He78)616706c4d6f7bdf68b30893f860cbb2b$$aFederico, Giuseppina$$b1
000181227 7001_ $$0P:(DE-HGF)0$$aMathow, Daniel$$b2
000181227 7001_ $$0P:(DE-HGF)0$$aRabionet, Mariona$$b3
000181227 7001_ $$0P:(DE-He78)c0c8df340d42c170a0fbb477f31da163$$aRampoldi, Francesca$$b4$$udkfz
000181227 7001_ $$0P:(DE-He78)659b67be544344052284c48f7d49c7cd$$aPopovic, Zoran$$b5
000181227 7001_ $$0P:(DE-He78)a0a16a2508287abe75725c2a00627ca2$$aVolz, Martina$$b6$$udkfz
000181227 7001_ $$0P:(DE-He78)743a4a82daab55306a2c88b9f6bf8c2f$$aHielscher, Thomas$$b7$$udkfz
000181227 7001_ $$0P:(DE-He78)a928ded2085c8911822370cad0b4a728$$aSandhoff, Roger$$b8$$udkfz
000181227 7001_ $$0P:(DE-He78)00a2ea610aee4a8fca32908fc3d02e91$$aGröne, Hermann-Josef$$b9$$eLast author
000181227 773__ $$0PERI:(DE-600)2560162-3$$a10.18632/oncotarget.22648$$gVol. 8, no. 65, p. 109201 - 109216$$n65$$p109201 - 109216$$tOncoTarget$$v8$$x1949-2553$$y2017
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