Project description:Transcriptional profiling of neuroblastoma cell line expressing the PML1 isoform. Two-condition experiment: PML1 IMR32 vs empty vector IMR32. Two biological replicates, dye-swapped.
Project description:Transcriptional profiling of Oct4, Sox2, Lin28 and Nanog (OSLN) reprogramming cell of empty vector compared to HIF2α over-expression at the early stage (day 12) and the late stage(day 30) using fibroblasts MRC5 and IMR90
Project description:HCT116 cells transfected with lentiviral vectors expressing two different N-BLR shRNAs (clones #3-1 and #4-7) and empty vector control
Project description:Transcriptional profiling of mouse HMLEN breast cancer cells (HMLE cells transformed with -Neu oncogene) stably tranduced with pLEX-MCS based lentivirus. Three groups were compared, Vector cells, SNAIL expressing cells; and SNAIL+FBXO11 expressing cells. SNAIL expression induced strong EMT phenotype while SNAIL/FBXO11 reversed cells back to epithelial cells.
Project description:Transcriptional profiling of E2F4 target genes upon overexpression of E2F4 and it cofactors 4 conditions; E2F4 overexpression vs mock, E2F4 and DP-1 overexpression vs mock, E2F4 and RBL2 overexpression vs mock, E2F4, DP-1, and RBL2 overexpression vs mock. 2 or 4 replicates for each experimental conditions
Project description:We performed genome-wide expression profiling of miRNAs in order to search for those significantly affected by ASH1 transduction in a lung cancer cell line.
Project description:In the present study, we found that EZH1 depletion in MYCN-amplified neuroblastoma cells resulted in significant cell death as well as xenograft inhibition. EZH1 depletion decreased the level of H3K27me1; the interaction and protein stabilization of MYCN and EZH1 appear to play roles in epigenetic transcriptional regulation. Transcriptome analysis of EZH1-depleted cells resulted in down-regulation of the cell cycle progression-related pathway. In particular, GSEA revealed down-regulation of reactome E2F-mediated regulation of DNA replication along with key genes of this process, TYMS, POLA2, and CCNA1. TYMS and POLA2 were transcriptionally activated by MYCN and EZH1-related epigenetic modification. Treatment with the EZH1/2 inhibitor UNC1999 also induced cell death, decreased H3K27 methylation, and reduced the levels of TYMS in NB cells. Previous reports indicated neuroblastoma cells are resistant to 5-fluorouracil (5-FU) and TYMS (encoding thymidylate synthetase) has been considered the primary site of action for folate analogues. Intriguingly, UNC1999 treatment significantly sensitized MYCN-amplified neuroblastoma cells to 5-FU treatment, suggesting that EZH inhibition may be an effective strategy for development of a new epigenetic treatment for neuroblastoma.