The DNAJC25 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the human DNAJC25 gene has been disrupted in the MES-OV ovarian cancer cell line. This polyclonal pool comprises a heterogeneous mixture of gene-edited cells, providing a robust loss-of-function model free from clonal selection biases. The polyclonal format captures a broad spectrum of editing events, making it particularly suitable for pooled functional genomics screens and for analyses that require representation of population-level responses.
MES-OV is an adherent epithelial cell line originally established from a human ovarian carcinoma. It is a widely utilized model for epithelial ovarian cancer, especially in research on chemoresistance mechanisms and tumor progression. MES-OV cells retain key characteristics of ovarian cancer, including intact stress-responsive signaling pathways and robust proliferative capacity. Their consistent growth and reproducible behavior in standard tissue culture conditions facilitate high-throughput drug screening and detailed mechanistic studies.
DNAJC25 encodes a J-domain co-chaperone that enhances the ATPase activity of HSP70, a central chaperone driving protein folding, translocation, and degradation. Through its J-domain, DNAJC25 directly interacts with HSP70 and also associates with HSP90, HOP, and CHIP, forming a complex that determines client protein fate. Its expression is transcriptionally regulated by heat shock factor 1 (HSF1) and upregulated by ER stress inducers such as tunicamycin and oxidative stress. DNAJC25 modulates the stability and function of client proteins including the kinase AKT and tumor suppressor p53, thereby influencing cell survival and apoptosis. Furthermore, it intersects with the unfolded protein response (UPR) by engaging with key sensors and effectors: the ER chaperone GRP78, the stress transducers ATF6, IRE1, and PERK, and the downstream effectors XBP1 and CHOP.
In the MES-OV ovarian cancer model, loss of DNAJC25 function is expected to impair the cellular capacity to resolve proteotoxic stress, thereby increasing vulnerability to chemotherapeutic agents that promote protein misfolding or ER stress. Ovarian carcinoma cells frequently exploit HSP70-mediated chaperone networks to survive therapeutic challenges; disruption of DNAJC25 likely attenuates AKT-dependent pro-survival signaling and dysregulates p53-mediated stress responses, shifting the balance toward apoptosis. Consequently, this knockout model provides a powerful system to investigate how co-chaperone dysfunction exacerbates drug sensitivity and compromises adaptive stress responses.
Typical applications include dissecting the contribution of DNAJC25 to chemoresistance using cell viability and drug sensitivity assays, and monitoring UPR activation through qPCR for downstream targets such as XBP1 and CHOP. Western blotting can assess changes in DNAJC25, HSP70, and client protein expression. Migration and apoptosis assays further enable investigation of DNAJC25??s role in cancer cell invasiveness and programmed cell death. These polyclonal cells are also well-suited for pooled screens to identify synthetic lethal interactions or modulators of proteotoxic stress. For further details or technical support, please contact Ascent Research.
