Project description:To uncover the dysregulated genes in BCa, we performed the RNA-seq to detect the gene expression levels in four BCa cells (5637, UMUC3, T24, and J82) and human immortalized urothelial cell SV-HUC-1. To search for the differentially expressed genes of for cell lines (5637, J82, UMUC3, and T24) compared to the normal cell line SV-HUC-1.
Project description:To detect the differential expressed proteins in bladder cancer(BCa)-derived exosomes, we isolated BCa cell-derived exosome and normal bladder epithelial cell-derived exosomes. The quantitative proteomics were conducted to detect the upregulated proteins in BCa cell-derived exosomes compared with SV-HUC-1-derived exosomes.
Project description:To further explore the differential expression profile of super-enhancer long noncoding RNA (LncRNA) in human bladder cancer, we have employed super-enhancer lncRNA microarray expression profiling as a discovery platform to identify potential differential expression profile of super-enhancer lncRNA between human bladder cancer cell (UM-UC-3 cell) and urothelial immortalized cell (SV-HUC-1 cell). Results showed that a large number of differentially expressed super-enhancer lncRNA were found between UM-UC-3 cell and SV-HUC-1 cell. In this study, We verified 5 up-regulated differentially expressed super-enhancer lncRNAs using qPCR, of which the highest fold change is LINC00162. Then we further explored the biological function and mechanism of LINC00162 in bladder cancer in this study.
Project description:RBM4 is a RNA-binding protein (RBP) able to modulate splicing by promoting exon inclusion and shares an import pathway with other splicing factors in the nucleus. In earlier studies we found that RBM4 interacts and colocalizes with WT1, which has been implicated in 10M-bM-^@M-^S15% of WilmsM-bM-^@M-^Y tumours and more recently in leukemya, is considered to be a tumour suppressor. RBM4, a RBP whose splicing effect is inhibited by the +KTS isoform of the tumour-suppressor/activator WT1, exhibits altered expression in different tumours, and may be essential for proliferation. Moreover, RBM4 binds to a number of RNAs of genes involved in acute myeloid leukaemia and cell cycle control. These results suggest that RBM4 may be involved in alternative splicing, tumorigenesis and particularly leukaemogenesis. To determine the endogenous transcripts that are targeted by RBM4 at the genome-wide level, we decided to perform exon microarray studies. RBM4-specific siRNA has been used for knockdown of RBM4 in HeLa cells. RNA was extracted using a Qiagen RNA extraction kit from untransfected, mock and siRNA-transfected HeLa cells and quality of RNA for microarray analysis was checked using a Bioanalyzer 2100 (Agilent Technologies). Experiments were run in triplicates.
Project description:To explore the role of RBM4 in esophageal squamous cell carcinoma cell,we performed high-throughput mRNA sequencing (mRNA-seq) in KYSE150 with stable knockdown of RBM4 by shRNA . We then performed gene expression profiling analysis using data obtained from RNA-seq of KYSE150 cells,three replicates were sequenced.
Project description:We overexpressed RBM4 in HeLa cells to study RBM4-regulated genes using RNA-seq technology, followed by bioinformatic analysis of target genes of RBM4-regulated transcriptional factors (TFs)
Project description:To identify which mRNAs bind to RBM4/HIF-2a Two PAR-CLIPs were performed: One of an RBM4 immunoprecipitation, and the other of a HIF-2a immunoprecipitation and excising the associated RBM4 band.
Project description:HUC model includes three cell lines: HUC-BC, HUC-PC, and MCT11. They were all originally derived from human uroepithelium. However, three cell lines have different malignant potential. We here performed micro array to examine the differences in gene expression among three cell lines.