Project description:To categorize gene loss events in enzalutamide-treated LNCaP cells, a genome-wide CRISPR knockout (KO) screen was performed. We quantified sgRNA abundance between initial and final timepoints in DMSO and enzalutamide treated cell populations
Project description:Genome-wide CRISPR-Cas9 knockout screen using TKOv1 sgRNA library was performed in isogenic RBM10-proficient and RBM10-deficient HCC827 cells.
Project description:Docetaxel chemotherapy in metastatic prostate cancer offers only a modest survival benefit due to emerging resistance. To identify candidate therapeutic gene targets, we applied a murine prostate cancer orthograft model that recapitulates clinical invasive prostate cancer in a genome-wide CRISPR/Cas9 screen under docetaxel treatment pressure.
Project description:To search for factors regulating neuronal differentiation, we performed a genome-wide loss-of-function CRISPR/Cas9 screen in haploid human ESCs. The regulators were identified by the quantification of depletion of their mutant clones within a pooled loss-of-function library upon neuronal differentiation.
Project description:Genome-wide CRISPR-Cas9 knockout screen using TKOv1 sgRNA library performed in isogenic RBM10-proficient and RBM10-deficient HCC827 cells.
Project description:Prostate cancer (PCa) is the most frequently diagnosed malignancy in men worldwide. Epigenetic regulation has been recognized as a main mechanism of cancer evolution. PRMT5 is the major type II protein arginine methyltransferase catalyzing the symmetric dimethylation of arginine in mammalian. PRMT5 is found upregulated in PCa. However, its exact functional contribution to prostate tumorigenesis is unknown. PRMT5 inhibition via pharmacological inhibition (EPZ015666) reduces stemness with paralleled differentiation and arrests cell cycle progression but without causing appreciable apoptosis.To understand the mechanisms of cell tolerance to PRMT5 inhibition and to identify potential pathways that function synergistically with EPZ015666, we performed a genome-wide CRISPR/Cas9 loss-of-function screen in the presence of EPZ015666. Our data unravel that many clinical-grade drugs of known oncogenic pathways can be repurposed to target castration-resistant PCa when used in synergy with EPZ015666 at low doses. Genome-wide CRISPR/Cas9 loss-of-function screen in the presence of EPZ015666 in DU145
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