The JAG2 Knockout SK-OV-3 Polyclonal Cells represent a CRISPR/Cas9-mediated polyclonal knockout cell population designed to disrupt the JAG2 gene in the human SK-OV-3 epithelial ovarian adenocarcinoma cell line. This product provides a powerful loss-of-function model for investigating the biological roles of the Jagged2 ligand, a key activator of Notch signaling. The polyclonal nature of the knockout pool ensures a heterogeneous editing profile, which can be advantageous in capturing a range of functional consequences without the clonal selection bias of monoclonal lines. Researchers can utilize these cells to study Jagged2-dependent phenotypes in ovarian cancer biology, including proliferation, apoptosis, and metastasis.
The SK-OV-3 host cell line originates from the ascites of a 64-year-old female patient with ovarian adenocarcinoma. It exhibits epithelial morphology and is characterized by aneuploidy, along with inherent resistance to chemotherapeutic agents such as cisplatin and doxorubicin. This cell line is widely employed as a model system for ovarian adenocarcinoma, particularly in studies focusing on oncogenic signaling pathways, metastatic progression, and mechanisms of chemoresistance. The SK-OV-3 background is therefore ideal for evaluating the impact of JAG2 knockout on tumor aggressiveness and drug response.
JAG2 encodes the Jagged2 protein, a transmembrane ligand for Notch receptors (NOTCH1?C3). Upon cell-cell contact, Jagged2 binding triggers proteolytic cleavage of Notch by ADAM17 and ??-secretase, releasing the Notch intracellular domain (NICD). NICD forms a transcriptional complex with RBP-J?? and MAML to drive expression of target genes such as HES1, HEY1, HES5, MYC, and CCND1. Jagged2-mediated Notch signaling intersects with multiple pathways including PI3K/AKT/mTOR and TGF-??, and is regulated by upstream factors like HIF-1?? and TWIST1. Downstream effects influence cell fate decisions, proliferation, apoptosis, and immune modulation.
In the context of ovarian cancer, JAG2 is often aberrantly expressed and contributes to malignant phenotypes through sustained Notch activation. The JAG2 knockout in SK-OV-3 cells provides a physiologically relevant platform to dissect Jagged2-driven oncogenic signaling. Disruption of JAG2 is expected to attenuate Notch pathway activity, leading to reduced expression of downstream targets such as HES1 and MYC, and impaired tumor cell proliferation and survival. Moreover, this model can shed light on the role of Jagged2 in mediating resistance to cisplatin and doxorubicin, as well as its involvement in the modulation of the tumor microenvironment and metastatic behavior.
Typical research applications include proliferation and apoptosis assays using MTT and flow cytometry (Annexin V, Ki-67), Notch reporter luciferase assays to measure pathway activity, Transwell migration and invasion studies, and co-culture experiments with Notch reporter cells. This knockout model is also valuable for drug sensitivity profiling, transcriptomic analysis (RNA-seq), and in vivo xenograft tumor growth assays. Analysis of protein expression via Western blotting (Jagged2, HES1, HEY1) and phospho-signaling (pAKT, pERK) can further elucidate the molecular consequences of JAG2 loss. For additional technical information, please contact Ascent Research.
