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:We profile gene expression upon circCDYL KD in HepG2 cells and in two bladder cancer cell lines J82 and UMUC3 as well as upon knockdown of the RNA binding proteins (RBP) GRWD1, IGF2BP1, and IGF2BP2 in J82 and UMUC3
Project description:RNA-Seq of circCDYL knockdown (KD) samples in HepG2, J82, and UMUC3 cells and of GRWD1, IGF2BP1, and IGF2BP2 knockdown (KD) samples in J82 and UMUC3 cells
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.