| pubmed-article:18281026 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18281026 | lifeskim:mentions | umls-concept:C0431085 | lld:lifeskim |
| pubmed-article:18281026 | lifeskim:mentions | umls-concept:C0596290 | lld:lifeskim |
| pubmed-article:18281026 | lifeskim:mentions | umls-concept:C0000975 | lld:lifeskim |
| pubmed-article:18281026 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:18281026 | lifeskim:mentions | umls-concept:C0599473 | lld:lifeskim |
| pubmed-article:18281026 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:18281026 | pubmed:dateCreated | 2008-3-31 | lld:pubmed |
| pubmed-article:18281026 | pubmed:abstractText | Elucidation of the mechanisms underlying potential anticancer drugs continues and unraveling these mechanisms would not only provide a conceptual framework for drug design but also promote use of natural products for chemotherapy. The biological effects of (1'S)-acetoxychavicol acetate ((S)-ACA) have been widely investigated. However, in most cases, a natural product or synthetic racemic compound was used in the study. In this study, we prepared (S)-ACA and its enantiomer (R)-ACA by a lipase-catalyzed esterification method and sought to determine the mechanisms of action of (S)-ACA and (R)-ACA in the growth inhibitory effect in Ehrlich ascites tumor cells (EATC). (S)-ACA caused an accumulation of tumor cells in the G1 phase of the cell cycle, which was accompanied by a decrease in phosphorylated retinoblastoma protein (Rb), an increase in Rb and a decrease in the phosphorylation of p27kip1. However, (R)-ACA caused an accumulation of tumor cells in the G2 phase of the cell cycle, an increase in hyperphosphorylated Rb and an increase in the phosphorylation of p27kip1. The results obtained in the present study demonstrate for the first time, to the best of our knowledge, that both (S)-ACA and (R)-ACA caused the inhibition of tumor cells growth but the inhibition was caused via different mechanisms. | lld:pubmed |
| pubmed-article:18281026 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18281026 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18281026 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18281026 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18281026 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18281026 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18281026 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18281026 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18281026 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18281026 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:18281026 | pubmed:issn | 0009-2797 | lld:pubmed |
| pubmed-article:18281026 | pubmed:author | pubmed-author:KennedyDavid... | lld:pubmed |
| pubmed-article:18281026 | pubmed:author | pubmed-author:Matsui-YuasaI... | lld:pubmed |
| pubmed-article:18281026 | pubmed:author | pubmed-author:AzumaHidekiH | lld:pubmed |
| pubmed-article:18281026 | pubmed:author | pubmed-author:NorikuraToshi... | lld:pubmed |
| pubmed-article:18281026 | pubmed:author | pubmed-author:Kojima-YuasaA... | lld:pubmed |
| pubmed-article:18281026 | pubmed:author | pubmed-author:HuangXuedanX | lld:pubmed |
| pubmed-article:18281026 | pubmed:author | pubmed-author:XuShenghuiS | lld:pubmed |
| pubmed-article:18281026 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18281026 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:18281026 | pubmed:volume | 172 | lld:pubmed |
| pubmed-article:18281026 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18281026 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18281026 | pubmed:pagination | 216-23 | lld:pubmed |
| pubmed-article:18281026 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
| pubmed-article:18281026 | pubmed:meshHeading | pubmed-meshheading:18281026... | lld:pubmed |
| pubmed-article:18281026 | pubmed:meshHeading | pubmed-meshheading:18281026... | lld:pubmed |
| pubmed-article:18281026 | pubmed:meshHeading | pubmed-meshheading:18281026... | lld:pubmed |
| pubmed-article:18281026 | pubmed:meshHeading | pubmed-meshheading:18281026... | lld:pubmed |
| pubmed-article:18281026 | pubmed:meshHeading | pubmed-meshheading:18281026... | lld:pubmed |
| pubmed-article:18281026 | pubmed:meshHeading | pubmed-meshheading:18281026... | lld:pubmed |
| pubmed-article:18281026 | pubmed:meshHeading | pubmed-meshheading:18281026... | lld:pubmed |
| pubmed-article:18281026 | pubmed:meshHeading | pubmed-meshheading:18281026... | lld:pubmed |
| pubmed-article:18281026 | pubmed:meshHeading | pubmed-meshheading:18281026... | lld:pubmed |
| pubmed-article:18281026 | pubmed:meshHeading | pubmed-meshheading:18281026... | lld:pubmed |
| pubmed-article:18281026 | pubmed:meshHeading | pubmed-meshheading:18281026... | lld:pubmed |
| pubmed-article:18281026 | pubmed:meshHeading | pubmed-meshheading:18281026... | lld:pubmed |
| pubmed-article:18281026 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18281026 | pubmed:articleTitle | (1'S)-Acetoxychavicol acetate and its enantiomer inhibit tumor cells proliferation via different mechanisms. | lld:pubmed |
| pubmed-article:18281026 | pubmed:affiliation | Department of Food and Human Health Sciences, Graduate School of Human Life Science, Osaka City University, 3-3-138 Sugimoto, Osaka 558 8585, Japan. | lld:pubmed |
| pubmed-article:18281026 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18281026 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:18281026 | lld:pubmed |
