CRISPR screen exploring resistance to AKTi (Capivasertib) in ER+ Breast Cancer in MCF7, T47D and CAMA-1 cell lines
A genome-wide CRISPR-Cas9 knockout screen was performed in the breast cancer cell lines T47D, MCF7, and CAMA-1 to identify genes modulating sensitivity and resistance to capivasertib, a selective AKT inhibitor. Cells were transduced with a CRISPR library, followed by treatment with capivasertib or vehicle control (DMSO). Guide RNA (sgRNA) enrichment and depletion were assessed via next-generation sequencing to determine gene-level effects on cell viability and drug response. Gene-level data are provided for the initial plasmid library, baseline, DMSO-treated controls, and post-capivasertib treatment across replicates.
A genome-wide CRISPR-Cas9 knockout screen was performed in the breast cancer cell lines T47D, MCF7, and CAMA-1 to identify genes modulating sensitivity and resistance to capivasertib, a selective AKT inhibitor. Cells were transduced with a CRISPR library, followed by treatment with capivasertib or vehicle control (DMSO). Guide RNA (sgRNA) enrichment and depletion were assessed via next-generation sequencing to determine gene-level effects on cell viability and drug response. Gene-level data are provided for the initial plasmid library, baseline, DMSO-treated controls, and post-capivasertib treatment across replicates.
European Bioinformatics Institute