The DNAJB14 Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human epithelial ovarian cancer cell line. This product provides a loss-of-function model for the DNAJB14 gene, which encodes a DnaJ co-chaperone critical for Hsp70-mediated protein quality control. The polyclonal nature of the knockout pool reflects a heterogeneous mixture of edited alleles, offering a robust system to study DNAJB14-dependent functions without clonal selection bias. This cell population is suitable for investigating the immediate consequences of DNAJB14 disruption within the context of ovarian carcinoma biology.
The A2780 host cell line originates from untreated ovarian tumor tissue of a patient with ovarian carcinoma and serves as a widely used model for epithelial ovarian cancer. A2780 cells retain key features of the disease, including oncogenic signaling pathways and stress response mechanisms. Their utility in drug resistance studies and cancer biology complements the functional interrogation of ER-associated processes mediated by DNAJB14. This parental line provides a physiologically relevant background for assessing the impact of chaperone network alterations in ovarian cancer cells.
DNAJB14 belongs to the HSP40/DnaJ family and functions as a co-chaperone that recruits Hsp70 chaperones (HSPA1A, HSPA8) to protein substrates in the endoplasmic reticulum. It is intimately involved in the unfolded protein response (UPR) and ER-associated degradation (ERAD) pathways. Under ER stress, the sensors ATF6, IRE1, and PERK activate downstream effectors such as BiP (HSPA5) and CHOP (DDIT3). DNAJB14 interacts directly with Hsp70 and collaborates with other DnaJ co-chaperones to facilitate folding of nascent polypeptides and target terminally misfolded proteins for proteasomal degradation. Disruption of DNAJB14 is predicted to impair this proteostasis network, potentially leading to accumulation of misfolded proteins and chronic ER stress. The transcription factor HSF1, which regulates chaperone expression, and the UPR transcription factor XBP1 are also linked to DNAJB14-mediated quality control.
In the A2780 ovarian cancer context, DNAJB14 knockout holds particular relevance for studying ER stress adaptation in tumors. Ovarian carcinoma cells frequently encounter proteotoxic stress due to high secretory demands and genomic instability, relying on robust chaperone systems for survival. Loss of DNAJB14 may enhance sensitivity to proteasome inhibitors or chemotherapeutics that exacerbate ER stress, making this model useful for exploring mechanisms of drug resistance. Additionally, it provides a platform to dissect how cancer cells balance UPR signaling between pro-survival and pro-apoptotic outputs, with potential implications for targeting protein homeostasis in ovarian cancer.
Researchers can employ these DNAJB14 knockout A2780 polyclonal cells in a variety of experimental workflows. Western blotting and RT-qPCR enable monitoring of UPR markers such as BiP and CHOP, while flow cytometry facilitates apoptosis assessment under pharmacological ER stress induction. Cell viability assays can be used in drug sensitivity screens to identify compounds that exploit ER stress vulnerabilities. Immunofluorescence staining of ER markers allows examination of ER morphology changes. Together, these assays support investigations into chaperone function, protein misfolding diseases, and the development of novel therapeutic strategies for ovarian cancer. For further details, please contact Ascent Research.
