pubmed-article:20418948 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20418948 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:20418948 | lifeskim:mentions | umls-concept:C0376358 | lld:lifeskim |
pubmed-article:20418948 | lifeskim:mentions | umls-concept:C0334227 | lld:lifeskim |
pubmed-article:20418948 | lifeskim:mentions | umls-concept:C1101610 | lld:lifeskim |
pubmed-article:20418948 | lifeskim:mentions | umls-concept:C1413173 | lld:lifeskim |
pubmed-article:20418948 | lifeskim:mentions | umls-concept:C1414223 | lld:lifeskim |
pubmed-article:20418948 | lifeskim:mentions | umls-concept:C0599894 | lld:lifeskim |
pubmed-article:20418948 | lifeskim:mentions | umls-concept:C1533691 | lld:lifeskim |
pubmed-article:20418948 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
pubmed-article:20418948 | lifeskim:mentions | umls-concept:C1514485 | lld:lifeskim |
pubmed-article:20418948 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:20418948 | pubmed:dateCreated | 2010-4-26 | lld:pubmed |
pubmed-article:20418948 | pubmed:abstractText | BACKGROUND: Previous work has shown reduced expression levels of let-7 in lung tumors. But little is known about the expression or mechanisms of let-7a in prostate cancer. In this study, we used in vitro and in vivo approaches to investigate whether E2F2 and CCND2 are direct targets of let-7a, and if let-7a acts as a tumor suppressor in prostate cancer by down-regulating E2F2 and CCND2. METHODOLOGY/PRINCIPAL: Findings Real-time RT-PCR demonstrated that decreased levels of let-7a are present in resected prostate cancer samples and prostate cancer cell lines. Cellular proliferation was inhibited in PC3 cells and LNCaP cells after transfection with let-7a. Cell cycle analysis showed that let-7a induced cell cycle arrest at the G1/S phase. A dual-luciferase reporter assay demonstrated that the 3'UTR of E2F2 and CCND2 were directly bound to let-7a and western blotting analysis further indicated that let-7a down-regulated the expression of E2F2 and CCND2. Our xenograft models of prostate cancer confirmed the capability of let-7a to inhibit prostate tumor development in vivo. CONCLUSIONS/SIGNIFICANCE: These findings help to unravel the anti-proliferative mechanisms of let-7a in prostate cancer. Let-7a may also be novel therapeutic candidate for prostate cancer given its ability to induce cell-cycle arrest and inhibit cell growth, especially in hormone-refractory prostate cancer. | lld:pubmed |
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pubmed-article:20418948 | pubmed:language | eng | lld:pubmed |
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pubmed-article:20418948 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:20418948 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20418948 | pubmed:issn | 1932-6203 | lld:pubmed |
pubmed-article:20418948 | pubmed:author | pubmed-author:QinWeijunW | lld:pubmed |
pubmed-article:20418948 | pubmed:author | pubmed-author:WangHeH | lld:pubmed |
pubmed-article:20418948 | pubmed:author | pubmed-author:WangTaoT | lld:pubmed |
pubmed-article:20418948 | pubmed:author | pubmed-author:WangFuliF | lld:pubmed |
pubmed-article:20418948 | pubmed:author | pubmed-author:ChenZhinanZ | lld:pubmed |
pubmed-article:20418948 | pubmed:author | pubmed-author:YangAngangA | lld:pubmed |
pubmed-article:20418948 | pubmed:author | pubmed-author:YuanJianlinJ | lld:pubmed |
pubmed-article:20418948 | pubmed:author | pubmed-author:QinWeiweiW | lld:pubmed |
pubmed-article:20418948 | pubmed:author | pubmed-author:MengPingP | lld:pubmed |
pubmed-article:20418948 | pubmed:author | pubmed-author:DongQingchuan... | lld:pubmed |
pubmed-article:20418948 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20418948 | pubmed:volume | 5 | lld:pubmed |
pubmed-article:20418948 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20418948 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20418948 | pubmed:pagination | e10147 | lld:pubmed |
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pubmed-article:20418948 | pubmed:year | 2010 | lld:pubmed |
pubmed-article:20418948 | pubmed:articleTitle | MicroRNA let-7a inhibits proliferation of human prostate cancer cells in vitro and in vivo by targeting E2F2 and CCND2. | lld:pubmed |
pubmed-article:20418948 | pubmed:affiliation | Department of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China. dongqc168@yahoo.com.cn | lld:pubmed |
pubmed-article:20418948 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:20418948 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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