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To investigate the relative expression of long non-coding RNA 00673 (lncRNA 00673) in hepatocellular carcinoma (HCC) and HCC cells and study its regulation on the malignant phenotype of HCC cells PATIENTS AND METHODS: Samples of HCC and adjacent tissues from January 2013 to December 2015 were collected. The expression level of lncRNA00673 in HCC tissues and cells was detected by quantitative Real-time polymerase chain reaction (qRT-PCR) assays. lncRNA00673 specific interference sequences were transiently transfected into HCC cells and the effect of HCC cells on the biological behavior of HCC cells was examined by in vitro experiments ((3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT assay), flow cytometry, transwell, etc.). A tumor model of nude mice with HCC was established for the study of tumor growth condition of tumor-bearing mice after the interference with lncRNA00673 expression. Changes in expression levels of molecular markers on Notch signaling pathway after the interference with lncRNA00673 were detected by Western blot.lncRNA00673 was highly expressed in HCC tissues and cells. MTT results showed that interfering with lncRNA00673 inhibited cell proliferation. Flow cytometry results showed that HCC cell cycle was retarded in G1-G0 phase, thus promoting apoptosis after the interference with lncRNA00673. Western blot results showed that expression levels of molecular markers on Notch signaling pathway were changed after the interference with lncRNA00763.lncRNA00673 is highly expressed in HCC tissues and cells, and can promote the proliferation and metastasis of HCC by the regulation on Notch signaling pathway. lncRNA00673 may be a potential target for the treatment of HCC.

Hepatitis C virus (HCV)-induced iron overload has been shown to promote liver fibrosis, steatosis, and hepatocellular carcinoma. The zonal-restricted histological distribution of pathological iron deposits has hampered the attempt to perform large-scale in vivo molecular investigations on the comorbidity between iron and HCV. Diagnostic and prognostic markers are not yet available to assess iron overload-induced liver fibrogenesis and progression in HCV infections. Here, by means of Spike-in SILAC proteomic approach, we first unveiled a specific membrane protein expression signature of HCV cell cultures in the presence of iron overload. Computational analysis of proteomic dataset highlighted the hepatocytic vitronectin expression as the most promising specific biomarker for iron-associated fibrogenesis in HCV infections. Next, the robustness of our in vitro findings was challenged in human liver biopsies by immunohistochemistry and yielded two major results: (i) hepatocytic vitronectin expression is associated to liver fibrogenesis in HCV-infected patients with iron overload; (ii) hepatic vitronectin expression was found to discriminate also the transition between mild to moderate fibrosis in HCV-infected patients without iron overload. © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.