The DNAJC5 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the MES-OV human ovarian endometrioid carcinoma cell line. This loss-of-function model disrupts the DNAJC5 gene, enabling functional studies of the encoded cysteine string protein alpha (CSP-alpha) in processes such as chaperone-assisted SNARE complex assembly and autophagy, without clonal selection bias.
MES-OV is an adherent epithelial cell line derived from a human ovarian endometrioid carcinoma, widely used as a model for ovarian cancer biology. The cells retain malignant epithelial features, including dysregulated signaling and altered stress responses, making them suitable for investigating tumor-intrinsic mechanisms. Incorporating a DNAJC5 knockout in this background allows examination of CSP-alpha??s role in ovarian cancer cell physiology, particularly under proteotoxic or autophagic challenge.
DNAJC5 encodes CSP-alpha, a co-chaperone for HSC70/HSPA8 that is regulated by PKA and HSF1 signaling and activated by cellular stress. CSP-alpha directly interacts with HSC70 and SNARE proteins Syntaxin-1, SNAP-25, and VAMP2 to facilitate synaptic vesicle exocytosis. Independently, it promotes autophagic clearance by recruiting LC3, p62/SQSTM1, and VCP/p97, coupling chaperone activity to degradation. These dual roles position DNAJC5 as a critical regulator of proteostasis and membrane trafficking.
In ovarian cancer, CSP-alpha??s functions in exocytosis and autophagy may influence tumor adaptation to stress, secretion of growth factors, and chemoresistance. Although DNAJC5 is primarily linked to CLN4 neurodegeneration, emerging evidence indicates that chaperone-mediated processes and autophagy contribute to ovarian tumor progression. By disrupting DNAJC5 in MES-OV cells, this model enables dissection of its potential tumor-modulatory roles, including effects on cell viability, autophagy flux, and SNARE-dependent secretion.
Researchers can utilize this knockout population for Western blotting, RT-qPCR, and autophagy flux assays with chloroquine treatment and LC3 puncta imaging. Co-immunoprecipitation with HSC70 or Syntaxin-1 can map altered protein interactions. It is also suitable for drug screens targeting autophagy modulators or investigating stress sensitization. Thus, these cells provide a versatile tool for studying CSP-alpha pathology in cancer and neurodegeneration. For further details, please contact Ascent Research.
