Nicotinamide phosphoribosyltransferase (NAMPT) is a rate-limiting enzyme in regenerating nicotinamide adenine dinucleotide (NAD þ ) from nicotinamide in mammals. NAMPT has crucial roles for many cellular functions by regulating NAD þ -dependent SIRT1 deacetylase. However, roles of NAMPT in cancer are poorly defined. In this study, we show that NAMPT is prominently overexpressed in human prostate cancer cells along with SIRT1. Elevation of NAMPT expression occurs early for the prostate neoplasia. Inhibition of NAMPT significantly suppresses cell growth in culture, soft agar colony formation, cell invasion and growth of xenografted prostate cancer cells in mice. NAMPT knockdown sensitizes prostate cancer cells to oxidative stress caused by H 2 O 2 or chemotherapeutic treatment. Overexpression of NAMPT increases prostate cancer cell resistance to oxidative stress, which is partially blocked by SIRT1 knockdown. We demonstrate that in addition to modulating SIRT1 functions, the NAMPT inhibition reduces forkhead box, class 'O' (FOXO)3a protein expression and its downstream anti-oxidant genes catalase and manganese superoxide dismutase. Our results suggest important roles of concomitant upregulation of NAMPT and SIRT1 along with increased FOXO3a protein level for prostate carcinogenesis and their contribution to oxidative stress resistance of prostate cancer cells. These findings may have implications for exploring the NAMPT pathway for prostate cancer prevention and treatment.

Weissella cibaria 110 was isolated from plaa-som, a Thai fermented fish product, and known to produce the weissellicin 110 bacteriocin. We carried out comprehensive comparative genomic analysis of W. cibaria 110 with four other non-bacteriocin-producing W. cibaria strains and identified potential antibiotic-resistant genes. We further identified a type III restriction-modification system, a TA system, and a bacteriocin gene cluster that are unique in W. cibaria 110. Genes related to bacteriocin biosynthesis are organized in clusters and are encoded with minimum genetic machinery consisting of structural cognate immunity genes, including ABC transporter and immunity protein. Finally, we predicted W. cibaria 110 to produce a class IId bacteriocin, weissellicin 110, which is 31 amino acids in length and contains a 21-amino-acid N-terminal leader peptide. This is the first bacteriocin-producing sequencing genome in W. cibaria, and we describe the difference between the bacteriocin-producing and non bacteriocin-producing strains from genome point of view.

A left atrial mass associated with coronary artery disease is often diagnosed as a mural thrombus rather than other possible etiologies such as benign primary cardiac tumor (myxoma, lipoma), a malignant primary cardiac tumor (sarcoma, lymphoma), or secondary involvement for extracardiac tumors. Malignant lymphoma initially presenting as intracardiac masses is very rare. Chest computed tomography with contrast enhancement and cardiac magnetic resonance may be the best methods for distinguishing primary cardiac tumors from direct extension from adjacent mediastinal structures. We report the case of a 59-year-old man with incidentally found mediastinal diffuse large B-cell lymphoma invading the left atrium, which presented with coronary artery disease and a left atrial mass. Improvement in cardiac ventricular function heart after coronary artery bypass grafting may provide the patient with a better chance of receiving an adequate dose of chemotherapy.

Nampt/visfatin acts in both intracellular and extracellular compartments to regulate multiple biological roles, including NAD metabolism, cancer, inflammation, and senescence. However, its function in chronic inflammation and carcinogenesis in hepatocellular carcinoma (HCC) has not been well-defined. Here we use Huh-7 hepatoma cells as a model to determine how Nampt/visfatin affects cellular survival under oxidative stress. We found that the transition of Nampt/visfatin from intracellular into extracellular form was induced by H2O2 treatment in 293T cells and confirmed that this phenomenon was not due to cell death but through the secretion of Nampt/visfatin. In addition, Nampt/visfatin suppressed cell viability in oxidative treatment in Huh-7 cells and acted on the inhibition of hepatoma cell growth. Oxidative stress also reduced the Nampt-mediated activation of NF-κB gene expression. In this study, we identify a novel feature of Nampt/visfatin which functions as an adipokine that can be secreted upon cellular stress. Our results provide an example to understand how adipokine interacts with chemotherapeutic treatment by oxidative stress in HCC.