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Hepatocellular carcinoma (HCC) is a common malignant tumor usually resistant to chemotherapy. MicroRNAs play important roles in modulation of carcinogenesis and chemoresistance, which miR-16 has been reported to mediate chemoresistance in many types of cancers. However, the role of miR-16 in HCC remains unknown. The aim of this study was to investigate whether miR-16 is participated in chemoresistance in HCC and shed light on the underlying molecular mechanisms. The findings of the current study discover that miR-16 is down-regulated in HCC tissue and cell lines. The results demonstrate that the inhibition of miR-16 renders resistance to paclitaxel in vitro and in vivo by targeting IKBKB via NF-κB signaling pathway, suggesting that miR-16 may be a meaningful therapeutic potential to overcome drug resistance in HCC. [ABSTRACT FROM AUTHOR]

Objective The aim of this study was to identify candidate pathogenic autoantigens of Behçet’s disease (BD) in pathogen-stimulated target cells. Methods First, three cell lines were used as target cells to screen autoantibody. Second, selected target cells were simulated with pathogens. Third, western blotting was used for detecting the auto-antigens in cell extracts. Next, immunoprecipitation was performed and the amino-acid sequences of target antigens were analyzed by LC-MALDI-TOF/TOF. Then, the potential target antigen was expressed, purified, and immunologically confirmed. And finally, an ELISA kit was developed and clinically validated through the assessments of 456 clinical samples with BD. Results One antigen with a molecular weight of approximately 27-kDa was identified as heat shock protein 27 (HSP27). The reactivity of serum IgG against recombinant human HSP27 was detected in 52 of 91 BD patients (57%), 66 of 92 rheumatoid arthritis (RA) patients (72%), 32 of 90 Sjogren syndrome (SS) patients (36%), 22 of 92 systemic lupus erythematosus (SLE) patients (24%) and 0 of 91 healthy controls (HC). The reactivity of BD serum IgG antibodies against HSP27 was significantly higher than SLE ( P < 0.0001) SS ( P < 0.0001) and HC ( P < 0.0001). Conclusions This study identified HSP27 as a candidate endothelial cell autoantigen of BD, which is interesting and probably worth further exploration. [ABSTRACT FROM AUTHOR]

Objective This study is intended to screen potential antigen for Behcet’s disease (BD) by using human microvascular endothelial cells (HUVEC). Methods Following cell-based indirect immunofluorescence assay with sera from BD patients, proteins extracted from HUVEC were separated and detected by Western blotting. Then the target protein was identified by LC-MALDI-TOF/TOF, the recombinant target protein was expressed, purified and then used as coating antigen to test the prevalence of autoantibodies in patient’s sera. Results The Western blotting result showed that some patients’ sera could react with a protein band with about 30 kDa of molecular weight, which was further identified as prohibitin by mass spectrometry. The prevalence of serum antibodies against recombinant human prohibitin was detected in 16 of 58 BD patients (28%) but none in healthy controls. [ABSTRACT FROM AUTHOR]

Abstract: Insulin-like growth factor binding protein-3 (IGFBP-3) is known to inhibit cell proliferation and induce apoptosis in IGF-dependent and IGF-independent manners, but the mechanism underlying IGF-independent effects is not yet clear. In a yeast two-hybrid assay, IGFBP-3 was used as the bait to screen a human fetal liver cDNA library for it interactors that may potentially mediate IGFBP-3-regulated functions. N-Acetylgalactosaminyltransferase 14 (GalNAc-T14), a member of the GalNAc-Tases family, was identified as a novel IGFBP-3 binding partner. This interaction involved the ricin-type beta-trefoil domain of GalNAc-T14. The interaction between IGFBP-3 and GalNAc-T14 was reconfirmed in vitro and in vivo, using GST pull-down, co-immunoprecipitation and mammalian two-hybrid assays. Our findings may provide new clues for further study on the mechanism behind the IGF-independent effects of IGFBP-3 promoting apoptosis. The role of GalNAc-T14 as an intracellular mediator of the effects of IGFBP-3 need to be verified in future studies. [Copyright &y& Elsevier]