The JAK1 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited population of A2780 ovarian carcinoma cells with targeted disruption of the JAK1 gene. This polyclonal knockout pool provides a heterogeneous loss-of-function model for studying JAK1-dependent signaling while avoiding clonal selection biases. The cells are ready for downstream molecular and functional analyses.
A2780 is a well-characterized human epithelial ovarian cancer cell line derived from an untreated patient, widely utilized in ovarian cancer pathogenesis and drug response research. Exhibiting features of high-grade serous carcinoma, with wild-type TP53 and sensitivity to chemotherapeutics and targeted inhibitors, it offers a clinically relevant model for investigating signaling pathways and therapeutic vulnerabilities.
JAK1 encodes a non-receptor tyrosine kinase central to JAK-STAT cytokine signaling. It associates with intracellular portions of type I/II cytokine receptors (e.g., IL-2R??, gp130) and becomes activated upon ligand binding by interferons-??/??, interleukins-2/6, and growth hormone. Activated JAK1 phosphorylates receptor chains and recruits STAT1, STAT3, STAT5A, and STAT5B, which are then phosphorylated, dimerize, and translocate to the nucleus to regulate genes including SOCS family members, c-Myc, c-Fos, IRF1, and PIM1. JAK1 cooperates with JAK2 and TYK2 and is negatively controlled by SOCS1, SOCS3, PIAS, and PTPN11.
In ovarian cancer, JAK1-driven signaling modulates proliferation, survival, migration, and immune evasion. Aberrant JAK-STAT activation, particularly STAT3, is common in ovarian tumors. JAK1 knockout in A2780 cells enables dissection of cytokine-mediated oncogenic mechanisms, assessment of JAK inhibitor specificity, and modeling of tumor cell responses to immune-derived interleukins and interferons, aiding studies on chemoresistance and tumor microenvironment interactions.
This polyclonal knockout tool supports a range of applications. Western blotting for phospho-STAT1/3/5 after cytokine stimulation (e.g., IL-6, IFN-??) verifies pathway ablation. RT-qPCR quantifies STAT target genes (c-Myc, SOCS3). Functional assays test proliferation, migration, and invasion with or without JAK inhibitors (ruxolitinib, tofacitinib). Co-immunoprecipitation examines JAK1-receptor complexes. RNA-seq defines global transcriptional changes. The product enables JAK-STAT pathway interrogation and JAK inhibitor validation in ovarian cancer. Please contact Ascent Research for technical support.
