Linked Life Data

20946116

Source:http://linkedlifedata.com/resource/pubmed/id/20946116

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2010-11-16
pubmed:abstractText
Indinavir, a human immunodeficiency virus (HIV) protease inhibitor, inhibits the growth of tumor cells in vivo but does not show any cytotoxicity against cancer cells in vitro. To optimize the anticancer activity of indinavir, two novel analogs, CH05-0 and CH05-10, were synthesized. CH05-10 was much more cytotoxic than indinavir and had similar cytotoxicity to nelfinavir, the one with the best anticancer activities among all HIV protease inhibitors examined. For 14 cell lines representing 10 different types of human malignancies, the 50% inhibitory concentration (IC(50)) values of CH05-10 are in the range of 4.64-38.87 ?M. Further detailed studies using the lung cancer cell line A549 as the model system showed that the effect of CH05-10 on the A549 cell line is both time- and dose-dependent. The CH05-10 treatment not only induced cell cycle arrest at G(1) and caused caspase-dependent apoptosis, but also resulted in caspase-independent death via the induction of endoplasmic reticulum stress and unfolded protein response. These findings demonstrate that CH05-10, a novel indinavir analog, is a potent anticancer agent with pleiotropic effects.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1349-7006
pubmed:author
pubmed:copyrightInfo
© 2010 Japanese Cancer Association.
pubmed:issnType
Electronic
pubmed:volume
101
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2644-51
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
CH05-10, a novel indinavir analog, is a broad-spectrum antitumor agent that induces cell cycle arrest, apoptosis, endoplasmic reticulum stress and autophagy.
pubmed:affiliation
Laboratory of Pathogen Biology, State Key Laboratory of Respiratory Disease, Center for Infection and Immunity, Institute of Chemical Biology, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Science Park, Guangzhou, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't