The DNAJC10 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A2780 ovarian endometrioid adenocarcinoma cell line. This loss-of-function model targets DNAJC10, an ER luminal redox-dependent chaperone and protein disulfide isomerase. The polyclonal format provides a heterogeneous mixture of edited cells, enabling robust functional studies of DNAJC10 in protein folding and ER stress responses without clonal biases.
A2780 is a widely used ovarian carcinoma cell line from an untreated endometrioid adenocarcinoma patient. These epithelial cells are frequently employed in drug sensitivity and resistance research, particularly with cisplatin and paclitaxel. Their well-characterized biology and assay compatibility make them an ideal host for investigating ER stress pathways in cancer.
DNAJC10 is transcriptionally activated by the UPR sensors ATF6 and XBP1s upon ER stress. It interacts with BiP/GRP78 and PDI family proteins to facilitate the folding of client proteins and to target misfolded substrates for ERAD. By reducing misfolded protein accumulation, DNAJC10 mitigates ER stress and promotes cell survival. It functions downstream of ER stress sensors, integrating adaptive responses.
In ovarian cancer, dysregulated ER stress signaling contributes to tumor progression and drug resistance. DNAJC10 knockout in A2780 cells provides a model to study how this chaperone influences cancer cell adaptation to proteotoxic stress. Loss of DNAJC10 may sensitize cells to ER stress inducers and alter chemosensitivity, revealing vulnerabilities in ovarian carcinoma.
Representative assays with these cells include Western blotting for UPR markers (BiP/GRP78, XBP1s), RT-qPCR for XBP1 splicing, cell viability assays under tunicamycin or thapsigargin treatment, Annexin V apoptosis assays, and migration/invasion studies. They are also suited for drug sensitivity screens with cisplatin and paclitaxel. For further information, please contact Ascent Research.
