Depletion of methionine aminopeptidase 2 does not alter cell response to fumagillin or bengamides

Inhibition of endothelial cell growth by fumagillin has been assumed to be mediated by inhibition of the molecular target methionine aminopeptidase 2 (MetAp2). New data show that depletion of MetAp2 by siRNA does not inhibit endothelial cell growth. Moreover, MetAp2-depleted endothelial cells remain...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 2004-05, Vol.64 (9), p.2984-2987
Main Authors: KIM, Sunkyu, LAMONTAGNE, Kenneth, SABIO, Michael, SHARMA, Sushil, VERSACE, Richard W, YUSUFF, Naeem, PHILLIPS, Penny E
Format: Article
Language:English
Subjects:
Aminopeptidases - antagonists & inhibitors
Aminopeptidases - deficiency
Aminopeptidases - genetics
Aminopeptidases - metabolism
Antineoplastic agents
Azepines - pharmacology
Biological and medical sciences
Carcinoma, Non-Small-Cell Lung - enzymology
Cell Division - drug effects
Cell Division - physiology
Cell Line, Tumor
Cyclohexanes
Endothelium, Vascular - drug effects
Endothelium, Vascular - enzymology
Enzyme Inhibitors - pharmacology
Fatty Acids, Unsaturated - pharmacology
Humans
Lung Neoplasms - enzymology
Medical sciences
Metalloendopeptidases - antagonists & inhibitors
Metalloendopeptidases - deficiency
Metalloendopeptidases - genetics
Metalloendopeptidases - metabolism
Pharmacology. Drug treatments
RNA, Small Interfering - genetics
Sesquiterpenes
Substrate Specificity
Transfection
Tumors
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Summary:Inhibition of endothelial cell growth by fumagillin has been assumed to be mediated by inhibition of the molecular target methionine aminopeptidase 2 (MetAp2). New data show that depletion of MetAp2 by siRNA does not inhibit endothelial cell growth. Moreover, MetAp2-depleted endothelial cells remain responsive to inhibition by either fumagillin or a newly identified MetAp2 enzyme inhibitor. These data suggest that MetAp2 function is not required for endothelial cell proliferation.
ISSN:0008-5472
1538-7445
DOI:10.1158/0008-5472.CAN-04-0019