Also, viral and nonviral vectors are being developed for optimized delivery of synthetic or expressed RNA to liver (51�C53). Hence, restoration of miR-99a could have considerable potential for HCC gene therapy. To sum up, by investigating the potential role of miR-99a in cell cycle control and tumor progression, we highlight miR-99a further info as a prognosis predictor, and restoration of miR-99a could be a prospective therapeutic approach for HCC. Supplementary Material Supplemental Data: Click here to view. Acknowledgments We appreciate the help from Maoshan Chen (Beijing Genomics Institute (BGI), Shenzhen) on informatics analysis. We also thank Dr. Minggang Zhang, Yan Gu, Shuo Ye, and Chaofeng Han, for helpful discussions and Panpan Ma, Mei Jin, and Yan Li for technical assistance.

*This work was supported by National 125 Key Project Grant 2012ZX10002-014, National Key Basic Research Program of China Grant 2012CB518903, National High Biotechnology Development Program of China Grant 2009ZX09503-003, National Natural Science Foundation of China Grant 31170826, and Shanghai Committee of Science and Technology Grant 10DZ1910300. The on-line version of this article (available at http://www.jbc.org) contains supplemental Tables 1�C3 and Figs. 1�C6. 3The abbreviations used are: miRNA microRNA HCC hepatocellular carcinoma mTOR mammalian target of rapamycin qRT quantitative RT AFP ��-fetoprotein DFS disease-free survival HBV hepatitis B virus NC negative control MTT 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide EdU 5-ethynyl-2��-deoxyuridine.

Inflammatory bowel disease (IBD) may lead to potentially severe complications and even mortality [1]. Although the exact etiology is unclear, it is thought to result from a combination of mucosal immune system dysregulation, hyper-reactivity against the intestinal microbiota, and a compromised intestinal epithelial barrier function in genetically predisposed individuals [2]. Genes associated with IBD highlight key pathogenic mechanisms, including disturbed anti-bacterial defense (e.g. NOD2, ATG16L1, cathelicidin, defensins) and barrier function (e.g. PARD3, MAGI2, myosin IXB) [3]-[8]. In recent genome-wide association studies, the total number of susceptibility loci amounts to 99, but this probably accounts for only 16% of the ulcerative colitis (UC) [9] and 20% of the Crohn’s disease (CD) heritability [10].

It has been estimated that future genome-wide association scans will only yield a few more percent of CD and UC heritability. Biological pathway-based analyses or studies focusing on genes involved in established or plausible pathogenetic Carfilzomib pathways may be an alternative approach [11]. The bile salt nuclear Farnesoid X Receptor (NR1H4, nuclear receptor subfamily 1, group H, member 4, alias FXR on chromosome 12q23.1) is a member of the superfamily of nuclear receptors.