| pubmed-article:12964001 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12964001 | lifeskim:mentions | umls-concept:C0063164 | lld:lifeskim |
| pubmed-article:12964001 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:12964001 | lifeskim:mentions | umls-concept:C1269955 | lld:lifeskim |
| pubmed-article:12964001 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:12964001 | lifeskim:mentions | umls-concept:C0243077 | lld:lifeskim |
| pubmed-article:12964001 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:12964001 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:12964001 | pubmed:dateCreated | 2003-9-9 | lld:pubmed |
| pubmed-article:12964001 | pubmed:abstractText | The mevalonate metabolic pathway is necessary for the isoprenylation of a number of small GTPases. We have previously presented that Rho plays a pivotal role in 1-oleoyl-lysophosphatidic acid (LPA)-induced invasion of rat ascites hepatoma MM1 cells. Herein we report the effect of HMG-CoA reductase inhibitors, fluvastatin and lovastatin, on the in vitro invasion of MM1 cells. Fluvastatin and lovastatin inhibited LPA-induced MM1 cell invasion in a dose-dependent manner. Fluvastatin inhibited LPA-induced translocation of RhoA protein from the cytosol to the membrane and RhoA activation which was measured by pull-down assay for GTP-bound RhoA. Fluvastatin also inhibited the translocation of both endogenous and dominant-active RhoA from the cytosol to the membrane, actin stress fiber assembly and in vitro invasion of the cells expressing dominant-active RhoA (Val14-RhoA). These results indicate that HMG-CoA reductase inhibitors have the potential to reduce RhoA activation and cancer cell invasion by targeting the Rho protein isoprenylation. | lld:pubmed |
| pubmed-article:12964001 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12964001 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12964001 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12964001 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12964001 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12964001 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12964001 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12964001 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12964001 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12964001 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12964001 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12964001 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12964001 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12964001 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12964001 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12964001 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12964001 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:12964001 | pubmed:issn | 1019-6439 | lld:pubmed |
| pubmed-article:12964001 | pubmed:author | pubmed-author:InoueMasahiro... | lld:pubmed |
| pubmed-article:12964001 | pubmed:author | pubmed-author:NakamuraHiroy... | lld:pubmed |
| pubmed-article:12964001 | pubmed:author | pubmed-author:MukaiMutsukoM | lld:pubmed |
| pubmed-article:12964001 | pubmed:author | pubmed-author:TatsutaMasaha... | lld:pubmed |
| pubmed-article:12964001 | pubmed:author | pubmed-author:KusamaToshiyu... | lld:pubmed |
| pubmed-article:12964001 | pubmed:author | pubmed-author:MatsumotoYosh... | lld:pubmed |
| pubmed-article:12964001 | pubmed:author | pubmed-author:ImamuraFumioF | lld:pubmed |
| pubmed-article:12964001 | pubmed:author | pubmed-author:AyakiMasakoM | lld:pubmed |
| pubmed-article:12964001 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12964001 | pubmed:volume | 23 | lld:pubmed |
| pubmed-article:12964001 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12964001 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12964001 | pubmed:pagination | 1173-8 | lld:pubmed |
| pubmed-article:12964001 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:12964001 | pubmed:meshHeading | pubmed-meshheading:12964001... | lld:pubmed |
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| pubmed-article:12964001 | pubmed:meshHeading | pubmed-meshheading:12964001... | lld:pubmed |
| pubmed-article:12964001 | pubmed:meshHeading | pubmed-meshheading:12964001... | lld:pubmed |
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| pubmed-article:12964001 | pubmed:meshHeading | pubmed-meshheading:12964001... | lld:pubmed |
| pubmed-article:12964001 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12964001 | pubmed:articleTitle | Inhibition of lysophosphatidic acid-induced RhoA activation and tumor cell invasion by 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors. | lld:pubmed |
| pubmed-article:12964001 | pubmed:affiliation | Department of Tumor Biochemistry, Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka 537-8511, Japan. kusama-to@mail.mc.pref.osaka.jp | lld:pubmed |
| pubmed-article:12964001 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12964001 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:12964001 | lld:pubmed |
