The DNAJB2 Knockout MES-OV Polyclonal Cells are a heterogeneous pool of MES-OV ovarian cancer cells in which the DNAJB2 gene has been disrupted via CRISPR/Cas9-mediated genome editing. This polyclonal knockout population provides a loss-of-function model for studying DNAJB2-dependent processes without the biases of single-cell cloning. The mixed genetic background better reflects the complexity of tumor cell populations and is well-suited for functional genomics, proteomics, and drug sensitivity studies.
The MES-OV cell line was established from a patient with ovarian adenocarcinoma and represents the mesenchymal molecular subtype, characterized by enhanced invasive and metastatic potential. This mesenchymal phenotype is associated with epithelial-to-mesenchymal transition (EMT) markers and inherent chemoresistance. Consequently, MES-OV cells serve as a robust model for investigating the molecular mechanisms underlying ovarian cancer progression, metastasis, and therapeutic resistance.
DNAJB2 encodes a J-domain co-chaperone that directly interacts with Hsp70 chaperones, primarily HSPA1A and HSPA8, to recognize and recruit misfolded or aggregation-prone client proteins. Under the regulation of HSF1 and cellular stress signals, DNAJB2 presents these substrates to the E3 ubiquitin ligase STUB1 (CHIP) for ubiquitination, thereby targeting them for degradation by the 26S proteasome. This pathway is central to the ubiquitin-proteasome system and collaborates with chaperone-mediated autophagy and ER-associated degradation. Knockout of DNAJB2 disrupts the chaperone-mediated triage, blocking efficient clearance of misfolded proteins and leading to the accumulation of ubiquitinated species and increased proteotoxic stress.
In MES-OV cells, which rely on robust proteostasis networks to sustain their invasive and metastatic behavior, loss of DNAJB2 function is expected to compromise stress adaptation and protein quality control. The mesenchymal ovarian cancer context is particularly relevant because cancer cells often exploit chaperone systems to survive hostile microenvironmental conditions. DNAJB2 disruption may sensitize these cells to proteotoxic insults, impair their migratory capacity, or alter their response to anticancer agents. This knockout model therefore offers a unique tool to probe the intersection between proteostasis and ovarian cancer malignancy.
These cells are suitable for a broad range of applications, including the study of chaperone-mediated protein degradation, proteasome activity, and aggregation-prone substrate clearance. Researchers can employ western blotting, immunoprecipitation, and immunofluorescence to analyze DNAJB2 pathway components, while proteasome activity and filter trap aggregation assays quantify functional consequences of the knockout. Combined with viability assays under heat shock or proteasome inhibitor treatment, the model enables investigation of stress response mechanisms in ovarian cancer. Transcriptomic and proteomic approaches such as RNA-seq can further elucidate global changes in the unfolded protein response. For additional information or to discuss customization, please contact Ascent Research.
