Anti-NDRG3 monoclonal antibody Made to order

Silurus asotus lectin (SAL) is a member of the rhamnose-binding lectin (RBL) family, and recognizes globotriaosylceramide (Gb3) on the cell surface of Burkitt's lymphoma cell lines, such as Raji and Daudi cells. The variation of gene expression in the treatment of both cells with SAL was analyzed using the differential display (DD) method with combination of 16 kinds of arbitary primers and 3 kinds of anchor primers. Treatment of Raji cells with SAL down-regulated mitochondria-associated granulocyte-macropharge colony-stimulating factor (GM-CSF) signaling molecule (Magmas) gene, and up-regulated N-myc downstream regulated gene (NDRG) 3. On the other hand, treatment of Daudi cells with SAL down-regulated Rad50 gene. Since Magmas gene expression was repressed in SAL-treated Raji cells, but did not change in SAL-treated D-threo-1-phenyl-2-decanoylamino-3-morphorino-1-propanol (PDMP)-pretreated Raji cells, it was clear that the expression of Magmas, NDRG3 or Rad50 was regulated by SAL binding to Gb3.

microRNAs (miRNAs) are short, non-coding RNAs with post-transcriptional regulatory functions that participate in diverse biological pathways. miR-122, a liver-specific miRNA, has been found to be down-regulated in hepatocellular carcinoma (HCC) and HCC-derived cell lines. In this study, miR-122 was down-regulated in the hepatitis B virus (HBV)-related HCC cell line HepG2.2.15 compared to HepG2. NDRG3, a member of the N-myc downstream-regulated gene (NDRG) family, was up-regulated in HepG2.2.15 and was identified as a target gene-Of miR-122. An inverse correlation between the expression of miR-122 and the NDRG3 protein was noted in HBV-related HCC specimens. The transfection of the miR-122 expression vector into the HepG2.2.15 cell line repressed the transcription and expression of NDRG3, which subsequently reversed the malignant phenotype of the cells. The replication of HBV, expression of viral antigens and proliferation of cells were significantly inhibited by restoration of miR-122. The data demonstrate that miR-122 plays an important role in HBV-related hepatocarcinogenesis by targeting NDRG3. Thus, miR-122 and NDRG3 represent key diagnostic markers and potential therapeutic targets for HBV-related HCC.