| pubmed-article:20368687 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20368687 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:20368687 | lifeskim:mentions | umls-concept:C0017638 | lld:lifeskim |
| pubmed-article:20368687 | lifeskim:mentions | umls-concept:C0008286 | lld:lifeskim |
| pubmed-article:20368687 | lifeskim:mentions | umls-concept:C0018270 | lld:lifeskim |
| pubmed-article:20368687 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:20368687 | lifeskim:mentions | umls-concept:C0249197 | lld:lifeskim |
| pubmed-article:20368687 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
| pubmed-article:20368687 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:20368687 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:20368687 | pubmed:dateCreated | 2010-5-31 | lld:pubmed |
| pubmed-article:20368687 | pubmed:abstractText | 2-Chloro-10-[3(-dimethylamino)propyl]phenothiazinemonohydrochloride (chlorpromazine) is a phenothiazine derivative used clinically to control psychotic disorders. It also exhibits an anticancer activity. Treatment with chlorpromazine (CPZ) results in cell-cycle arrest at the G2/M phase in rat C6 glioma cells. CPZ reduces the expression of cell cycle-related proteins, such as cyclin D1, cyclin A, and cyclin B1, but causes an increase in the p21(Waf1/Cip1) level. The molecular mechanism by which CPZ regulates p21(Waf1/Cip1) expression is unknown. Here, we provide evidence that CPZ activates the p21(Waf1/Cip1) gene promoter via induction of the transcription factor early growth response-1 (Egr-1) independently of p53 in C6 cells. A point mutation in the Egr-1-binding motif within the p21(Waf1/Cip1) promoter abrogated promoter inducibility due to CPZ. Forced expression of Egr-1 enhanced p21(Waf1/Cip1) promoter activity. In contrast, knockdown of endogenous Egr-1 by small interference RNA attenuated CPZ-induced p21(Waf1/Cip1) promoter activity. A chromatin immunoprecipitation assay demonstrated that Egr-1 binds to the p21(Waf1/Cip1) gene promoter. Further analysis showed that the ERK and JNK MAP kinases are required for induction of Egr-1 by CPZ. Finally, stable silencing of Egr-1 expression lead to attenuated CPZ-inducible p21(Waf1/Cip1) expression and inhibited G2/M phase cell-cycle arrest. These results demonstrate that a functional link between ERK and JNK MAP kinase pathways and p21(Waf1/Cip1) induction via Egr-1 contributes to CPZ-induced anticancer activity in C6 glioma cells. | lld:pubmed |
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| pubmed-article:20368687 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20368687 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20368687 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20368687 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20368687 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20368687 | pubmed:month | May | lld:pubmed |
| pubmed-article:20368687 | pubmed:issn | 1226-3613 | lld:pubmed |
| pubmed-article:20368687 | pubmed:author | pubmed-author:ShinSoon... | lld:pubmed |
| pubmed-article:20368687 | pubmed:author | pubmed-author:LeeYoung... | lld:pubmed |
| pubmed-article:20368687 | pubmed:author | pubmed-author:LimYoonghoY | lld:pubmed |
| pubmed-article:20368687 | pubmed:author | pubmed-author:KimYong SikYS | lld:pubmed |
| pubmed-article:20368687 | pubmed:author | pubmed-author:KimSe HyunSH | lld:pubmed |
| pubmed-article:20368687 | pubmed:author | pubmed-author:KimChang... | lld:pubmed |
| pubmed-article:20368687 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:20368687 | pubmed:day | 31 | lld:pubmed |
| pubmed-article:20368687 | pubmed:volume | 42 | lld:pubmed |
| pubmed-article:20368687 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20368687 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20368687 | pubmed:pagination | 395-405 | lld:pubmed |
| pubmed-article:20368687 | pubmed:dateRevised | 2010-9-28 | lld:pubmed |
| pubmed-article:20368687 | pubmed:meshHeading | pubmed-meshheading:20368687... | lld:pubmed |
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| pubmed-article:20368687 | pubmed:meshHeading | pubmed-meshheading:20368687... | lld:pubmed |
| pubmed-article:20368687 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:20368687 | pubmed:articleTitle | Chlorpromazine activates p21Waf1/Cip1 gene transcription via early growth response-1 (Egr-1) in C6 glioma cells. | lld:pubmed |
| pubmed-article:20368687 | pubmed:affiliation | Institute of Biomedical Science and Technology, Konkuk University Hospital, Seoul 143-729, Korea. | lld:pubmed |
| pubmed-article:20368687 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:20368687 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
