The DNAJC1 Knockout MES-OV Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal cell population derived from the MES-OV human ovarian endometrioid carcinoma cell line, with targeted disruption of the DNAJC1 gene. This product provides a versatile loss-of-function model for investigating the molecular functions of DNAJC1, a DnaJ domain-containing co-chaperone. The polyclonal knockout pool, obtained via CRISPR/Cas9-mediated genome editing, offers a heterogeneous population of edited cells that facilitates the study of gene function without clonal selection biases. This cellular model is suitable for researchers examining the role of DNAJC1 in endoplasmic reticulum (ER) stress responses, chaperone networks, and apoptotic signaling.
The parental MES-OV cell line is an established model of ovarian endometrioid carcinoma, a subtype of epithelial ovarian cancer. MES-OV cells retain key characteristics of their tumor origin, including epithelial morphology and oncogenic signaling pathways. This cell line has been widely employed in ovarian cancer research, providing a relevant context for investigating tumorigenesis, metastasis, and therapeutic sensitivities. The endometrioid histological subtype is associated with distinct molecular features, and the MES-OV line serves as a representative system for exploring endometriosis-associated ovarian cancer biology and ER stress-dependent survival mechanisms.
DNAJC1 functions as a critical co-chaperone that stimulates the ATPase activity of Hsp70, thereby regulating protein folding, translocation, and degradation, particularly under ER stress. It is an integral component of the unfolded protein response (UPR) network, acting downstream of the ER stress sensors IRE1, PERK, and ATF6, and transcriptionally regulated by HSF1 and XBP1. DNAJC1 physically interacts with Hsp70, as well as co-chaperones and modulators including HOP, CHIP, and BAG family proteins, forming part of a dynamic chaperone cycle. By modulating Hsp70 activity, DNAJC1 influences the folding and stability of client proteins and exerts indirect control over the Bcl-2 family of apoptosis regulators and downstream caspase activation. In this capacity, DNAJC1 contributes to the balance between adaptive stress responses and pro-apoptotic signaling mediated by CHOP and GRP78/BiP.
In the context of ovarian endometrioid carcinoma, the ER stress and UPR pathways are frequently dysregulated and contribute to cancer cell survival, proliferation, and chemoresistance. Disruption of DNAJC1 in MES-OV cells compromises the cell’s ability to mount an effective cytoprotective response, rendering them more susceptible to ER stress-induced apoptosis. This knockout model therefore provides a valuable tool for dissecting how co-chaperone activity modulates UPR outcomes in ovarian cancer. It enables the investigation of DNAJC1-dependent mechanisms in tumor cell adaptation and may inform studies on synthetic lethal interactions or sensitization to ER stress-inducing therapeutics.
Researchers can utilize this polyclonal knockout cell pool in a wide array of applications, including the validation of co-chaperone functions, dissection of UPR signaling branches, and assessment of apoptosis regulation. Representative experimental approaches include Western blotting and RT-qPCR to quantify UPR marker expression (e.g., CHOP, GRP78), RNA-seq for global transcriptional profiling, co-immunoprecipitation to probe DNAJC1-interacting protein complexes, and apoptosis assays (Annexin V/PI). Functional assays such as MTT, colony formation, and drug response studies can evaluate the impact of DNAJC1 loss on ovarian cancer cell viability and treatment sensitivity. For further technical details, please contact Ascent Research.
