The BAG5 Knockout SK-OV-3 Polyclonal Cells represent a genetically disrupted cell population generated via CRISPR/Cas9-mediated genome editing, targeting the BAG5 gene in the human SK-OV-3 ovarian adenocarcinoma cell line. This polyclonal knockout pool provides a heterogeneous loss-of-function model, suitable for studying BAG5-dependent pathways without clonal selection artifacts.
SK-OV-3 is a well-characterized human ovarian adenocarcinoma cell line isolated from the malignant ascites of a patient with high-grade serous ovarian cancer. These adherent epithelial cells harbor a TP53 mutation and are widely used to model aggressive ovarian cancer, including studies of chemoresistance, tumor progression, and metastasis.
BAG5 encodes a co-chaperone that binds the Hsp70/Hsc70 molecular chaperones, inhibiting their ATPase activity and modulating protein folding, autophagy, and apoptosis. In the context of mitophagy, BAG5 blocks parkin-mediated mitochondrial clearance by interfering with the PINK1/parkin pathway, thereby promoting cell survival under stress. BAG5 interacts with multiple partners including Hsp70, Hsc70, Parkin, DJ-1, CHIP, and Bcl-2, and its expression is regulated by the HSF1 transcription factor upon heat shock or cellular stress, positioning it at the intersection of proteostasis and mitochondrial quality control.
Disruption of BAG5 in SK-OV-3 cells creates a powerful tool to investigate its role in ovarian cancer biology, particularly the mechanisms underlying chemoresistance. BAG5 overexpression has been implicated in the survival of cancer cells following cisplatin treatment, and its knockout is expected to sensitize cells to apoptosis by restoring parkin-dependent mitophagy and modulating Bcl-2 family protein interactions. This model therefore enables precise dissection of BAG5’s anti-apoptotic functions in a disease-relevant cellular background.
This knockout cell population is suitable for a variety of experimental applications, including Western blotting and co-immunoprecipitation to probe protein interactions, mitophagy flux assays with LC3 and Parkin, MTT viability and Annexin V apoptosis assays to assess chemosensitivity, and migration/invasion studies to gauge metastatic potential. Additionally, CRISPR editing can be validated by Sanger sequencing, and the polyclonal nature facilitates pooled screening approaches. For further information, please contact Ascent Research.
