Project description:To test the hypothesis that the propensity for silencing of tumor suppressor genes in the respiratory epithelium of chronic smokers by promoter hypermethylation is influenced by sequence variations that modify the activity of genes and microRNAÕs that directly or indirectly influence de novo methylation and chromatin remodeling.
Project description:In this study, we aimed to characterize the suppressive role of NCOA6 in prostate cancer development, uncover the underlying molecular mechanism, and identify potential therapeutic targets for treating NCOA6 loss-induced prostate cancer. Gene expression microarray analysis and RNA-Seq analysis were performed to identify differentially expressed genes influenced by NCOA6 in 22Rv1 human prostate cancer cells and mouse prostate tumors, respectively. Pathway enrichment analysis and gene set enrichment analysis were performed to identify NCOA6-regulated signaling pathways, particually the cancer-associated pathways. ChIP-Seq analysis was further performed to identify NCOA6-associated genomic regions in 22Rv1 cells. The potential direct target genes of NCOA6 were identified by combined analysis of the gene expression profiling data and ChIP-Seq data. Finally, we identified EGFR as one of the 264 NCOA6 direct target genes and deomonstrated that NCOA6 suppressed prostate cancer progression by preventing EGFR overexpression.
Project description:An increasing number of studies have demonstrated that miRNAs may act as oncogenes or anti-oncogenes in various types of cancer, including colon carcinoma (CC). However the clinical and biological significance of miR663a in the prognosis of CC and its underlying mechanisms remain unknown. In our study, it was found that miR663a was significantly downregulated in CC, especially in metastatic CC tissues. MiR663a overexpression not only inhibited the proliferation and migration/invasion of CC cells in vitro, but also inhibited tumor growth and metastasis of CC cells in vivo. However the mechanism under that was still unknown. So miR663a target genes were analyzed in our project.
Project description:To investigate biological function of MARVELD1, we have employed whole genome microarray expression profiling as a platform to analyze gene expression alternation influenced by MARVELD1. MARVELD1 stably transfected NIH3T3 and control vector cells were used to compare their gene expression profiling.
