Project description:We performed RNA-seq analysis on xenograft mouse model generated by T24 human bladder cancer cell line with enforced expression of DDR1 or controls.
Project description:We knocked down SOX4 in T24 cell and created 3 cell lines: T24-scrambled, T24-SOX4-knockdown and T24-SOX4-rescue and compared gene expression changes SOX4 is a developmental transcription factor that is overexpressed in as many as 23% of bladder cancer patients, but the role of SOX4 in bladder cancer tumorigenesis is not well understood. Given SOX4’s many roles in embryonic development and context-dependent regulation of gene expression, we sought to understand SOX4’s contribution to bladder cancer and to elucidate SOX4 regulated genes that might contribute to tumorigenesis. We employed a CRISPR interference (CRISPRi) method to transcriptionally repress SOX4 expression in T24 bladder cancer cell lines, rescued these cell lines with lentivirally expressed SOX4, and performed whole genome expression profiling. SOX4 knockdown cells exhibited decreased invasive capabilities but no changes in migration or proliferation, while rescue with SOX4 lentiviral vector restored the invasive phenotype. Gene expression profiling revealed 173 high confidence SOX4 regulated genes
Project description:To identify DNA accessibility targets regulated by the SWI/SNF subunit SMARCB1 in bladder cancer, we compared the ATAC-seq signals in T24 cells engineered for SMARCB1 knockout, non-targeting control, or SMARCB1 re-expression following knockout. Analysis of altered DNA accessibility profiles revealed new roles for SMARCB1 in the regulation of gene expression in bladder cancer, and suggested new therapeutic opportunities.
Project description:Target genes regulated by G9a in bladder cancer cells T24 In this dataset, we include the expression data obtained from bladder cancer cells T24 treated with G9a siRNA or negative control siRNA. These data are used to obtain genes that are differentially expressed in response to G9a konckdown.
Project description:Target genes regulated by ox-LDL treatment in bladder cancer cells T24 were identified by microarrays. In this dataset, we include the expression data obtained from bladder cancer cells T24 starved with serum-free medium and then treated with 20 μg/mL ox-LDL or vehicle for 24 h. These data are used to obtain genes that are differentially expressed in response to ox-LDL treatment.
Project description:We established stable miR-146a-5p overexpression T24 cells, then performed transcriptome profiling of miR-146a-5p overexpressing cells compared to control T24 cells to detect the molecular mechanisms of the miR-146a-5p’s effect on bladder cancer cells.
Project description:TRAF4 is highly expressed in the epithelial bladder cancer cell line, HT1376 and poorly expressed in the mesenchymal cell line, T24. We evaluated the genetic changes in HT1376 upon TRAF4 knockdown using two independent shRNAs targetting TRAF4. The changes were documented with respect to the control cell line transduced with empty vector shRNA plasmid. Also, we over-expressed (myc-tagged) TRAF4 in T24 and evaluated mRNA changes with respect to cell line over-expressing empty vector with a myc-tag.
Project description:UBC9 is the sole conjugating enzyme E2 in the sumoylation and plays a pivotal role in maintaining homeostasis and restraining stress reaction. Targeting UBC9 is emerging as a novel strategy for cancer therapy. However, the role of UBC9 in bladder cancer is not clear. Here, we sought to determine the alterations of trancriptome after shRNA-mediated knockdown UBC9 in T24 cell lines.
Project description:To investigate the difference of mRNA and lncRNA profiling between cisplatin-resistance and regular T24 bladder cancer cells, T24 cells were treated with a gradual increment (4, 8, 16, 32, 64 ug/ml cisplatin) with a discontinuous period until cells recover. 10^6 cells T24R and T24 cells were harvested for RNA-seq.