Project description:Our observation suggest that ADAR may play important role to maintain GSC stemness. In order to address this hypothesis, we abrogated the expression of ADAR in GSCs using two distinct short and non-overlapping shot hairpin RNAs (shRNAs). A non-targeting control shRNA (shCONT) is used as control in these experiments. Both shRNAs significantly reduced ADAR protein expression. Depletion of ADAR impaired GSCs proliferation but did not affect matched DGCs. Similarly, lack of ADAR reduces GSC self-renewal capacity as assessed by in vitro limiting dilution assay . In order to identify the antitumor mechanisms triggered by ADAR depletion, we performed global transcriptional profiling through RNA-sequencing in GSCs upon ADAR knockdown. These analyses show that ADAR downregulation impairs the impairs the expression of genes involved in cancer proliferation, particularly those involved in cell cycle regulation
Project description:To unravel the molecular function of TAPIR-1 and -2, four different specific siRNAs were used to knockdown the TAPIR-transcripts in LNCaP-cells. Gene expression changes upon knockdown of TAPIR was assessed by Agilent SurePrint G3 Human Gene Expression Arrays at 24h and 48h after treatment.
Project description:RNA sequencing on LNCaP cells was carried out to study how tunicamycin-induced gene expression is affected by knockdown of EIF2AK3 and ATF4.
Project description:LNCaP cells were transfected with 3 different REST siRNAs Transcriptomics analysis was performed to compare gene expression changes induced by REST knockdown
Project description:LNCaP cells were transfected with 3 different REST siRNAs Transcriptomics analysis was performed to compare gene expression changes induced by REST knockdown Genome-wide transcriptomic analysis of LNCaP cells transfected with REST siRNA
Project description:Quantitative proteomic analysis of tumor tissue lysates from wildtype LNCaP (WT) and LNCaP OR51E2-/- (KO) xenografts in male CIEA NOG mice.
