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dc.contributor.authorZhang, Siwei
dc.contributor.authorSchneider, Lina S
dc.contributor.authorVick, Binje
dc.contributor.authorGrunert, Michaela
dc.contributor.authorJeremias, Irmela
dc.contributor.authorMenche, Dirk
dc.contributor.authorMüller, Rolf
dc.contributor.authorVollmar, Angelika M
dc.contributor.authorLiebl, Johanna
dc.date.accessioned2016-07-12T10:56:50Z
dc.date.available2016-07-12T10:56:50Z
dc.date.issued2015-12-22
dc.identifier.citationAnti-leukemic effects of the V-ATPase inhibitor Archazolid A. 2015, 6 (41):43508-28 Oncotargeten
dc.identifier.issn1949-2553
dc.identifier.pmid26496038
dc.identifier.doi10.18632/oncotarget.6180
dc.identifier.urihttp://hdl.handle.net/10033/615979
dc.description.abstractPrognosis for patients suffering from T-ALL is still very poor and new strategies for T-ALL treatment are urgently needed. Our study shows potent anti-leukemic effects of the myxobacterial V-ATPase inhibitor Archazolid A. Archazolid A reduced growth and potently induced death of leukemic cell lines and human leukemic samples. By inhibiting lysosomal acidification, Archazolid A blocked activation of the Notch pathway, however, this was not the mechanism of V-ATPase inhibition relevant for cell death induction. In fact, V-ATPase inhibition by Archazolid A decreased the anti-apoptotic protein survivin. As underlying mode of action, this work is in line with recent studies from our group demonstrating that Archazolid A induced S-phase cell cycle arrest by interfering with the iron metabolism in leukemic cells. Our study provides evidence for V-ATPase inhibition as a potential new therapeutic option for T-ALL.
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleAnti-leukemic effects of the V-ATPase inhibitor Archazolid A.en
dc.typeArticleen
dc.contributor.departmentHelmholtz-Institute for Pharmaceutical Research Saarland (HIPS),Saarland 9 University, 66123 Saarbrücken, Germany.en
dc.identifier.journalOncotargeten
refterms.dateFOA2018-06-13T19:33:57Z
html.description.abstractPrognosis for patients suffering from T-ALL is still very poor and new strategies for T-ALL treatment are urgently needed. Our study shows potent anti-leukemic effects of the myxobacterial V-ATPase inhibitor Archazolid A. Archazolid A reduced growth and potently induced death of leukemic cell lines and human leukemic samples. By inhibiting lysosomal acidification, Archazolid A blocked activation of the Notch pathway, however, this was not the mechanism of V-ATPase inhibition relevant for cell death induction. In fact, V-ATPase inhibition by Archazolid A decreased the anti-apoptotic protein survivin. As underlying mode of action, this work is in line with recent studies from our group demonstrating that Archazolid A induced S-phase cell cycle arrest by interfering with the iron metabolism in leukemic cells. Our study provides evidence for V-ATPase inhibition as a potential new therapeutic option for T-ALL.


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