The JAK3 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the A2780 human ovarian carcinoma cell line. This loss-of-function model is generated through CRISPR/Cas9-mediated disruption of the JAK3 gene, creating a heterogeneous cell pool with targeted gene ablation. The polyclonal format avoids clonal artifacts and enables robust population-level studies. These cells serve as a ready-to-use tool for dissecting JAK3-dependent signaling and evaluating JAK3 as a therapeutic target in ovarian cancer.
The A2780 parental cell line is an epithelial ovarian cancer model established from an untreated patient??s ovarian endometrioid adenocarcinoma. It exhibits hallmark features of high-grade serous carcinoma, including aberrant cytokine signaling and unchecked proliferation. A2780 is extensively used for functional assays, drug screening, and pathway analysis, with its reliance on JAK-STAT signaling making it ideal for interrogating JAK3 function.
JAK3 is a non-receptor tyrosine kinase that associates with the common gamma chain (IL2RG) of receptors for IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21. Upon ligand binding, JAK3 is activated and phosphorylates STAT5, STAT3, and STAT1. These transcription factors dimerize and translocate to the nucleus to induce MYC, CCND1, and BCL2L1, which promote cell cycle progression and survival. JAK3 acts in concert with JAK1 and SHC1, and its signaling converges with PI3K-AKT and MAPK pathways to amplify proliferative signals.
In A2780 ovarian cancer cells, JAK3-driven STAT signaling supports proliferation and survival, with IL-2 stimulation activating the JAK3/STAT5 axis and upregulating oncogenic targets. Disruption of JAK3 in this polyclonal knockout model abrogates cytokine-dependent STAT phosphorylation and downstream transcriptional programs, attenuating tumorigenic phenotypes. This system provides a physiologically relevant platform for studying JAK3 loss-of-function and its role in ovarian cancer pathogenesis.
These knockout cells can be used in western blotting for JAK3 and phospho-STAT5, RT-qPCR for MYC and CCND1, MTT viability assays, flow cytometry for apoptosis (Annexin V/PI), colony formation assays, IL-2 cytokine stimulation with phospho-signaling analysis, and drug sensitivity testing with JAK inhibitors like tofacitinib. The model is suited for target validation, signaling dissection, and preclinical evaluation of JAK3-targeted therapies in ovarian cancer. For further information, please contact Ascent Research.
