Project description:Background: Liver cancer is the third deadliest type of cancer, posing a serious threat to human health. Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer. C. sinensis, classified as a definite group I carcinogen by the IARC (International Agency for Research on Cancer), is an important risk factor for HCC. Although many studies have shown that C. sinensis infection affects the prognosis of HCC patients, the specific mechanisms are still unclear, especially the dynamics and regulatory roles of chromatin accessibility. Results: In this study, we integrated ATAC-seq, RNA-seq, and ChIP-seq data to elucidate changes in the epigenetics of HCC after the C. sinensis infection. Many different accessibility regions (DARs) were identified both in tumors and adjacent tissue after the C. sinensis infection. Meanwhile, top TFs whose motifs were enriched in DAR were found, such as HNF4a, FOXI1, etc. Although there were slight deviations, epigenetic changes were found to be consistent with gene expression levels. We also revealed that H3K9ac, H3K4me2, H3K4me3, H3K27ac, and H3K4me1 were associated with chromatin accessibility. Importantly, we also found potential evidence that C. sinensis infection would alter the spatial structure of the HCC genome. Finally, both molecular experimental results and clinical data certified that C. sinensis infection would promote the metastasis of HCC. Conclusions: C. sinensis infection will remodel the chromatin accessibility of HCC, leading to changes in gene expression levels. This study provides conclusive evidence that C. sinensis infection alters the epigenetics of HCC.
Project description:Rgg-dependent transcriptional regulation in SF370 Streptococcus pyogenes strain was analyzed during post-exponential phase of growth Keywords: rgg mutant
Project description:Streptococcus agalactiae, also known as Group B streptococcus, emerged in the 1960s as a leading cause of septicemia and meningitis in neonates. It is also an increasing cause of infections in adults with underlying diseases. To characterize transcription start sites (TSS) in the hypervirulent ST17 lineage (strain BM110) we used a differential RNA-seq strategy, based on selective Tobacco Acid Pyrophosphatase (TAP) treatment and adapter ligation, which differentiates primary transcripts and processed RNAs
