2.50
Hdl Handle:
http://hdl.handle.net/10033/615979
Title:
Anti-leukemic effects of the V-ATPase inhibitor Archazolid A.
Authors:
Zhang, Siwei; Schneider, Lina S; Vick, Binje; Grunert, Michaela; Jeremias, Irmela; Menche, Dirk; Müller, Rolf ( 0000-0002-1042-5665 ) ; Vollmar, Angelika M; Liebl, Johanna
Abstract:
Prognosis 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.
Affiliation:
Helmholtz-Institute for Pharmaceutical Research Saarland (HIPS),Saarland 9 University, 66123 Saarbrücken, Germany.
Citation:
Anti-leukemic effects of the V-ATPase inhibitor Archazolid A. 2015, 6 (41):43508-28 Oncotarget
Journal:
Oncotarget
Issue Date:
22-Dec-2015
URI:
http://hdl.handle.net/10033/615979
DOI:
10.18632/oncotarget.6180
PubMed ID:
26496038
Type:
Article
Language:
en
ISSN:
1949-2553
Appears in Collections:
publications of the department of microbial natural substances ([HIPS]MINS)

Full metadata record

DC FieldValue Language
dc.contributor.authorZhang, Siweien
dc.contributor.authorSchneider, Lina Sen
dc.contributor.authorVick, Binjeen
dc.contributor.authorGrunert, Michaelaen
dc.contributor.authorJeremias, Irmelaen
dc.contributor.authorMenche, Dirken
dc.contributor.authorMüller, Rolfen
dc.contributor.authorVollmar, Angelika Men
dc.contributor.authorLiebl, Johannaen
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.en
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

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