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pubmed-article:19472311 | lifeskim:mentions | umls-concept:C0016055 | lld:lifeskim |
pubmed-article:19472311 | lifeskim:mentions | umls-concept:C2239176 | lld:lifeskim |
pubmed-article:19472311 | lifeskim:mentions | umls-concept:C0027627 | lld:lifeskim |
pubmed-article:19472311 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
pubmed-article:19472311 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:19472311 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
pubmed-article:19472311 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:19472311 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:19472311 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:19472311 | pubmed:dateCreated | 2009-8-4 | lld:pubmed |
pubmed-article:19472311 | pubmed:abstractText | It is increasingly clear that hepatocellular carcinoma (HCC) has a distinct microRNA (miRNA) expression profile that is involved in malignancy; however, little is known about how functional miRNA modulates the metastasis of hepatitis B virus (HBV)-related HCC (HBV-HCC). In the present study, we demonstrate that the levels of miRNA-143 (miR-143) are dramatically increased in metastatic HBV-HCC of both p21-HBx transgenic mice and HCC patients. Moreover, we show that overexpression of this miRNA is transcribed by nuclear factor kappa B (NF-kappaB) and favors liver tumor cell invasive and metastatic behavior. Intratumoral administration of miR-143 shows that high levels of miR-143 can significantly promote HCC metastasis in an athymic nude mouse model. An in vivo study that used p21-HBx transgenic mice also showed that local liver metastasis and distant lung metastasis are significantly inhibited by blocking miR-143. Additionally, fibronectin type III domain containing 3B (FNDC3B), which regulates cell motility, was identified as the direct and functional target of miR-143 both in vivo and in vitro. CONCLUSION: Up-regulation of miR-143 expression transcribed by NF-kappaB in HBV-HCC promotes cancer cell invasion/migration and tumor metastasis by repression of FNDC3B expression. The present study provides a better understanding of the specificity of the biological behavior and thus may be helpful in developing an effective treatment against HBV-HCC. | lld:pubmed |
pubmed-article:19472311 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19472311 | pubmed:language | eng | lld:pubmed |
pubmed-article:19472311 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19472311 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:19472311 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19472311 | pubmed:month | Aug | lld:pubmed |
pubmed-article:19472311 | pubmed:issn | 1527-3350 | lld:pubmed |
pubmed-article:19472311 | pubmed:author | pubmed-author:ShuhanSunS | lld:pubmed |
pubmed-article:19472311 | pubmed:author | pubmed-author:HeYingY | lld:pubmed |
pubmed-article:19472311 | pubmed:author | pubmed-author:ZhangXiaoying... | lld:pubmed |
pubmed-article:19472311 | pubmed:author | pubmed-author:LiuShanrongS | lld:pubmed |
pubmed-article:19472311 | pubmed:author | pubmed-author:LiuShupengS | lld:pubmed |
pubmed-article:19472311 | pubmed:author | pubmed-author:HuTingsongT | lld:pubmed |
pubmed-article:19472311 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19472311 | pubmed:volume | 50 | lld:pubmed |
pubmed-article:19472311 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19472311 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19472311 | pubmed:pagination | 490-9 | lld:pubmed |
pubmed-article:19472311 | pubmed:dateRevised | 2009-9-2 | lld:pubmed |
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pubmed-article:19472311 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19472311 | pubmed:articleTitle | Up-regulated microRNA-143 transcribed by nuclear factor kappa B enhances hepatocarcinoma metastasis by repressing fibronectin expression. | lld:pubmed |
pubmed-article:19472311 | pubmed:affiliation | Department of Medical Genetics, Second Military Medical University, Shanghai, PR China. | lld:pubmed |
pubmed-article:19472311 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:19472311 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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