Activated monocytes produce a variety of cytokines that are involved in inflammation, such as IL-1, TNF, chemotactic factors, transforming growth factor R, platelet-derived growth factor, and IFN-a and -Q (1). Chemotactic factors released at foci of injury or bacterial invasion are thought to mediate directed migration of leukocytes into inflammatory sites. Since the leukocyte composition of the inflammatory infiltrate depends on the temporal stage of the lesion (2) and the nature of the stimulus (3), it follows that some chemoattractants should be specific for a given type of leukocyte. We recently showed that LPS-stimulated monocytes produce a chemotactic factor that attracts neutrophils, but not monocytes (4). We purified this factor to homogeneity and described the N1-12-terminal sequence of the first 42 amino acids (5). We now report molecular cloning and sequencing ofthe full-length cDNA for this monocyte-derived neutrophil chemotactic factor (MDNCF)' and the deduced amino acid sequence of the entire molecule. Specific cDNA probes also enabled us to test the capacity of a number of cytokines to induce MDNCF mRNA expression in human PBMC. The stimulation of MDNCF mRNA expression by IL-1 and TNF suggests that the local pro-inflammatory action of these cytokines may be mediated by induction of chemotactic factor secretion. Volume 167 June 1988 1883-1893 Materials and Methods cDNA Cloning of MDNCF and Nucleotide Sequence . Normal human PBMC were first fractionated by Ficoll-Hypaque and plastic adherent cells (> 90% nonspecific esterase-positive monocytes), were cultured in RPMI-1640 medium supplemented with 1% FCS and 10 ug/ml LPS (Serotype 055:1155; Difco Laboratories Inc., Detroit, MI) for 6 h at 37°C . Total RNA

These data highlight an important role for miR-124 in the regulation of invasion and metastasis in the molecular aetiology of HCC, and suggest a potential application of miR-124 in prognosis prediction and cancer treatment.

The most severe form of brain glioma, glioblastoma (GBM), is highly malignant and usually resistant to chemotherapy. Therefore, discovery of new targets for gene therapy is important. Using subtraction cloning, we identified the human N-Myc downstream-regulated gene 2 (hNDRG2), located at chromosome 14q11.2, as a gene that is significantly suppressed in GBM tissues. Semiquantitative RT-PCR showed that the hNDRG2 gene transcript is expressed in normal brain tissue and low-grade gliomas but is present at low levels in 15 of 27 (56%) human GBM tissues and all of the 6 human glioblastoma cell lines examined. Furthermore, transfection of human glioblastoma U373 and U138 cells with a cDNA encoding hNDRG2 markedly reduced the cell proliferation. Our findings provide the first evidence to suggest that hNDRG2 may play a role in glioblastoma carcinogenesis.

Background: B-lymphoma Moloney murine leukemia virus insertion region-1 (Bmi-1) acts as an oncogene in various tumors, and its overexpression correlates with a poor outcome in several human cancers. Ectopic expression of Bmi-1 can induce epithelial-mesenchymal transition (EMT) and enhance the motility and invasiveness of human nasopharyngeal epithelial cells (NPECs), whereas silencing endogenous Bmi-1 expression can reverse EMT and reduce the metastatic potential of nasopharyngeal cancer cells (NPCs). Mouse xenograft studies indicate that coexpression of Bmi-1 and H-Ras in breast cancer cells can induce an aggressive and metastatic phenotype with an unusual occurrence of brain metastasis; although, Bmi-1 overexpression did not result in oncogenic transformation of MCF-10A cells. However, the underlying molecular mechanism of Bmi-1-mediated progression and the metastasis of breast cancer are not fully elucidated at this time.