2 research outputs found
Regulating Action of in Vitro Hepatitis C Virus Infection on Interferon-Induced Interferon Stimulating Genes in Murine Macrophages
Objectives: The objective of this study was to determine the in vitro regulating effect of Hepatitis C virus (HCV) infection on interferon stimulating genes (ISGs) stimulated by IFN-Ò¯ and Imiquimod (TLR7 ligand) on murine macrophages. iNOS and STAT1 were measured by RT-PCR, and immunoblotting (IB). Nitric oxide production was measured by Griess Reagent Assay. Objectives: The objective of this study was to determine the in vitro regulating effect of Hepatitis C virus (HCV) infection on interferon stimulating genes (ISGs) stimulated by IFN-Ò¯ and Imiquimod (TLR7 ligand) on murine macrophages. iNOS and STAT1 were measured by RT-PCR, and immunoblotting (IB). Nitric oxide production was measured by Griess Reagent Assay. Results: HCV inhibits IFN induced iNOS mRNA and also protein expression. HCV significantly reduced IFN-Ò¯ induced ISGs (iNOS mRNA, iNOS protein, s727-STAT1, tyr701- STAT1). Conclusion: These results indicate that in vitro hepatitis C virus infection is involved in the regulation of IFN-Ò¯ induced ISGs in the levels of gene and protein expression of iNOS and STAT1 transcription factors.: HCV inhibits IFN induced iNOS mRNA and also protein expression. HCV significantly reduced IFN-Ò¯ induced ISGs (iNOS mRNA, iNOS protein, s727-STAT1, tyr701- STAT1). Conclusion: These results indicate that in vitro hepatitis C virus infection is involved in the regulation of IFN-Ò¯ induced ISGs in the levels of gene and protein expression of iNOS and STAT1 transcription factors
ABERRANT METHYLATION OF DPP6 IN LUNG ADENOCARCINOMA
We previously performed the genome‑wide screening of aberrantly methylated CpG islands (CGIs) using the paired tumorous and non‑tumorous tissues of 12 lung adenocarcinomas (LADC). In comparisons with paired normal lung tissues, dipeptidyl peptidase‑like 6 (DPP6) has been identified as the most significantly hypermethylated CGI in LADC. DPP6 is a protein that modulates A‑type potassium channels in the somatodendritic compartments of neurons, which play a role in synaptic plasticity. Previous studies have showed that DPP6 is downregulated in cancers, such as acute myeloid leukemia and melanoma, but upregulated in colon cancer, which is attributed to hyper‑ and hypomethylation, respectively. The present study investigated the methylation and expression levels of DPP6 and its prognostic value in patients with LADC. The DNA methylation and mRNA expression levels of DPP6 in surgically resected LADC tissues were examined by bisulfite pyrosequencing and reverse transcription‑quantitative PCR, respectively. The DNA methylation and mRNA expression levels of DPP6 were both significantly higher in LADC tissues compared with in normal lung tissues (n=25; P<0.0001). Overall and disease‑free survival rates were significantly higher in LADC with high mRNA expression levels compared with those with low levels. In conclusion, epigenetic alterations in DPP6 were significantly higher in LADC tissues compared with in normal lung tissues, which may contribute to the malignant features and worse prognosis of these patients