Stougaard Benjamin (oysterclave8)

Inorganic arsenicals are worldwide environmental contaminants that affect molecular characteristics in biological systems and lead to genomic and epigenomic instability as well as epithelial mesenchymal transition (EMT). In this study, we aimed to investigate whether low levels of sodium arsenite (iAsIII) can influence EMT and genomic instability through microsatellite analysis. We have also determined epigenomic instability by investigating the methylation status of SEPT9 tumor marker in colorectal cancer (CRC) cell lines, Caco2 and HCT116, which were treated with iAsIII to assess IC50s. Short-term and long-term exposure to low concentrations (1 µM and 0.1 µM) of iAsIII in two separate experiments was implemented to analyze EMT, microsatellite status and the methylation pattern of SEPT9 promoter. As expected, after 20 days of exposure to iAsIII, the expression of CDH1 was significantly decreased while the expression of CDH2, FIB1 and VIM was increased in Caco2 and HCT116, a finding that confirmed EMT induction. However, there was no detectable alteration in the size of microsatellites. As for the methylation pattern, SEPT9 promoter was hypomethylated as a result of long-term exposure to 0.1 µM iAsIII in Caco2. Long-term exposure of HCT116 to both concentrations could induce hypomethylation of SEPT9 promoter. Our findings indicate no linkage between EMT induction and microsatellite status in iAsIII-treated CRC cell lines. For the first time, the current study has shown that the induction of EMT by iAsIII is linked with SEPT9 promoter hypomethylation in Caco2 and HCT116 in a concentration- and time-dependent pattern.Circulating microRNAs have been recognized as promising biomarkers for the detection of lung cancer. The objective of this study was to evaluate miR-10b, miR-1 and, miR-30a in the plasma samples of lung cancer patients to confirm any possible relevance in the early detection of lung cancer. Plasma samples from 47 non-small-cell lung cancer patients and 41 cancer-free subjects were evaluated for selected microRNAs using the real-time PCR method. To evaluate the tobacco smoking effects on microRNAs expression, the studied groups were categorized into two subgroups never-smokers and smokers. MiR-1/miR-30a expression levels were significantly reduced in lung cancer, while the miR-10b level was significantly elevated. We found that smoking had significant effects on the levels of circulating microRNAs in the smokers of the cancer-free group (a significant up-regulation of miR-10b and significant down-regulation of miR-1/miR-30a), and lung cancer patients (a significant elevation of miR-10b). Receiver operating characteristic curve analysis showed that miR-10b with an area under the curve of 0.861, and miR-1/miR-30a with values of0.905 and 0.889 for the same parameter, could distinguish non-small-cell lung cancer patients from cancer-free subjects. Our findings demonstrated significant differences in the expression of microRNAs in lung cancer and the considerable effects of smoking on microRNAs levels. SR59230A mw Area under curve analysis showed that miR-10b with 78% sensitivity/78% specificity, miR-1 with 95% sensitivity/80% specificity and miR-30a with 87% sensitivity/83% specificity,might be good (miR-10b/miR-30a) and excellent (miR-1) markers for lung cancer detection.Early diagnosis of prostate cancer (PCa) as the second most common cancer in men is not associated with precise and specific results. Thus, alternate methods with high specificity and sensitivity are needed for accurate and timely detection of PCa. MicroRNAs regulate the molecular pathways involved in cancer by targeting multiple genes. The aberrant expression of the microRNAs has been reported in different cancer types including PCa. In this bioinformatics study, we studied differential expression profiles of microRNAs and their target genes in four PCa gene expression omnibus (GEO) databases. PCa diagnostic biomarker candidates were investigated u