Project description:Circular RNAs (circRNAs) have been increasingly indicated to be important participants in the development and progression of various malignant tumors. In this study, we analyzed circRNA high-throughout sequencing from human bladder cancer tissues and paired adjacent normal tissues. Then we focused on the upregulated circRNAs and identified a novel circular RNA, hsa_circ_0008399 , as a new candidate circRNA derived from RBM2 gene. FISH assay has been proved that hsa_circ_0008399 mainly located in nucleus. Transcriptome analysis was performed to find the potential genes that could be regulated by hsa_circ_0008399.
Project description:In order to find out circular RNAs profiles in human bladder cancer tissues and normal bladder tissues, we characterized circuclar RNA transcripts by performing RNA-Seq on ribosomal RNA-depleted total RNA from three pairs of human bladder cancer tissues and paired normal bladder tissues.A computational pipeline based on the anchor alignment of unmapped reads was used to identify circular RNAs. Collectively, we identified16,535 distict circular RNAs, most of them origined from exons (88.96%), others from introns, linc RNA, intergenic region, 3’UTR and 5’UTR. Among all these circRNAs, 571 circRNAs were differentially expressed between bladder cancer tissues and normal bladder tissues, and 524 circRNAs were downregulated in bladder cancer tissues (91.2%), others were upreguluated. These significantly differential expressed circular RNA might have regulatory function in bladder cancer, and worth to be further explored.
Project description:In this research, Human OneArray Microarray analysis was performed to obtain broad spectrum information about the genes differentially expressed in human bladder cancer cell line RT112 and Gemcitabine Resistant Bladder Cancer cell line RT112-Gr.
Project description:This is a comprehensive genomic characterization of 40 urothelial bladder carcinoma (UBC) cell lines including information on origin, mutation status of genes implicated in bladder cancer (FGFR3, PIK3CA, TP53, and RAS), copy number alterations assessed using high density SNP arrays, uniparental disomy (UPD) events, and gene expression. Based on gene mutation patterns and genomic changes we identify lines representative of the FGFR3-driven tumor pathway and of the TP53/RB tumor suppressor-driven pathway. High-density array copy number analysis identified significant focal gains (1q32, 5p13.1-12, 7q11, and 7q33) and losses (i.e. 6p22.1) in regions altered in tumors but not previously described as affected in bladder cell lines. We also identify new evidence for frequent regions of UPD, often coinciding with regions reported to be lost in tumors. Previously undescribed chromosome X losses found in UBC lines also point to potential tumor suppressor genes. Cell lines representative of the FGFR3-driven pathway showed a lower number of UPD events. Overall, there is a predominance of more aggressive tumor subtypes among the cell lines. We provide a cell line classification that establishes their relatedness to the major molecularly-defined bladder tumor subtypes. The compiled information should serve as a useful reference to the bladder cancer research community and should help to select cell lines appropriate for the functional analysis of bladder cancer genes, for example those being identified through massive parallel sequencing. Expression levels were assessed in 20 bladder cell lines, included in the UBC-40 Urothelial Bladder Cell Line Index, with Affymetrix U133 array platform
Project description:This is a comprehensive genomic characterization of 40 urothelial bladder carcinoma (UBC) cell lines including information on origin, mutation status of genes implicated in bladder cancer (FGFR3, PIK3CA, TP53, and RAS), copy number alterations assessed using high density SNP arrays, uniparental disomy (UPD) events, and gene expression. Based on gene mutation patterns and genomic changes we identify lines representative of the FGFR3-driven tumor pathway and of the TP53/RB tumor suppressor-driven pathway. High-density array copy number analysis identified significant focal gains (1q32, 5p13.1-12, 7q11, and 7q33) and losses (i.e. 6p22.1) in regions altered in tumors but not previously described as affected in bladder cell lines. We also identify new evidence for frequent regions of UPD, often coinciding with regions reported to be lost in tumors. Previously undescribed chromosome X losses found in UBC lines also point to potential tumor suppressor genes. Cell lines representative of the FGFR3-driven pathway showed a lower number of UPD events. Overall, there is a predominance of more aggressive tumor subtypes among the cell lines. We provide a cell line classification that establishes their relatedness to the major molecularly-defined bladder tumor subtypes. The compiled information should serve as a useful reference to the bladder cancer research community and should help to select cell lines appropriate for the functional analysis of bladder cancer genes, for example those being identified through massive parallel sequencing. Copy Number Variations were assessed in 45 bladder cell lines, included in the UBC-40 Urothelial Bladder Cell Line Index, with Human1M-Duov3 DNA Analysis BeadChip platform