求JBC和ELSEVIER的文献两篇，链接已附上，多谢！

sykbod

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2 ?$ w# v) \0 s4 O, u6 w3 E0 y; c第一篇JBC的：http://www.ncbi.nlm.nih.gov/pubmed/20463022?dopt=Abstract
5 S. ?8 f4 |/ s) e第二篇ELSEVIER的：http://www.ncbi.nlm.nih.gov/pubmed/18555017/* e2 K: U( V2 Y& o, V

5 C  v3 Z& f' Y3 H- V5 r* @8 o多谢！

hstudent

1 ok ok
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( e, a0 l7 F, tPro-tumorigenic effects of miR-31 loss in mesothelioma

inankai

Gastroenterology. 2008 Jul;135(1):257-69. Epub 2008 Apr 11.
/ S% m# e1 x9 yMicroRNA-223 is commonly repressed in hepatocellular carcinoma and potentiates expression of Stathmin1.
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$ e* {; U* H  X$ ]8 AWong QW, Lung RW, Law PT, Lai PB, Chan KY, To KF, Wong N.6 B- Y) V. z/ q9 s# t# R8 R: R1 n

- e3 M. e) ?# i% R6 gDepartment of Anatomical and Cellular Pathology at the Li Ka-Shing Institute of Health Sciences, The Chinese University of Hong Kong, SAR Hong Kong, China.
  @$ @. i/ N/ Z. d" Y& ]% T6 cAbstract
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5 L# B- e% F1 C! d7 T! p$ i+ RBACKGROUND & AIMS: Recent studies have emphasized causative links between microRNA (miRNA) deregulations and cancer development. In hepatocellular carcinoma (HCC), information on differentially expressed miRNA remained largely undefined." Q4 N! q  E7 J6 e+ I/ P' L$ W
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METHODS: Array-based miRNA profiling was performed on HCC cells that were derived from chronic carriers of hepatitis B virus (HBV) and hepatitis C virus (HCV), and nonviral-associated patients. Specific microRNA (miR)-223 and miR-222 deregulations were verified in an independent series of tumors. The functional effect of miR-223 was examined further. An integrative analysis of messenger RNA (mRNA) array with in silico predictions defined potential downstream targets of miR-223. A luciferase reporter assay was conducted to confirm target association.
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6 @* R1 z6 q5 ~5 m% fRESULTS: Distinct up-regulations of miR-222, miR-221, and miR-31, and down-regulations of miR-223, miR-126, and miR-122a were identified. Further investigations suggested the highly deregulated miR-223 and miR-222 could unequivocally distinguish HCC from adjacent nontumoral liver, irrespective of viral associations (P <or= .0002). Re-expression of miR-223 in HBV, HCV, and non-HBV non-HCV-related HCC cell lines revealed a consistent inhibitory effect on cell viability (P < .01). Integrative analysis further implicated Stathmin 1 (STMN1) as a downstream target of miR-223. A strong inverse relationship between STMN1 mRNA and miR-223 expressions was shown (P = .006). A substantial reduction in STMN1 protein was further demonstrated upon restoration of miR-223 expression in HCC cell lines. We further showed that miR-223 readily could suppress the luciferase activity in reporter construct containing the STMN1 3' untranslated region (P = .02).