The JAK2 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the A2780 human ovarian carcinoma epithelial cell line, featuring targeted disruption of the JAK2 gene. This loss-of-function model enables precise investigation of JAK2-dependent signaling in an epithelial ovarian cancer context. The polyclonal format provides a heterogeneous pool of edited cells, appropriate for studying gene function without clonal bias.
The A2780 host cell line was established from an untreated patient with ovarian endometrioid adenocarcinoma and exhibits an epithelial morphology. Widely employed in ovarian cancer research, A2780 cells are inherently sensitive to cisplatin, making them a valuable system for examining chemoresistance mechanisms and signaling networks that govern tumor cell proliferation and survival. This parental line has been extensively characterized in studies of ovarian carcinoma biology.
JAK2 encodes a non-receptor tyrosine kinase that is essential for hematopoiesis and immune cell development, acting downstream of numerous cytokine receptors including EPOR, TPOR, G-CSFR, IFNGR, and IL-6R family members. Upon ligand binding, JAK2 becomes activated and phosphorylates STAT transcription factors??principally STAT3 and STAT5??which then dimerize and translocate to the nucleus to regulate target gene expression. JAK2 signaling also engages the PI3K-AKT, MAPK/ERK, and NF-??B pathways, connecting to downstream effectors such as AKT, mTOR, ERK1/2, MYC, and BCL2 family proteins. The kinase interacts with cytokine receptor chains (e.g., GP130, ??c, ??c), adaptor proteins (SH2B family), and regulatory proteins (SOCS, PTPN11/SHP2) that modulate signal output. Representative pathway components include JAK2, STAT3, STAT5, GP130, SOCS3, PI3K, AKT, and ERK1/2.
In A2780 ovarian carcinoma cells, JAK2-dependent signaling supports proliferation, survival, and potentially contributes to chemoresistance and immune evasion. Abrogation of JAK2 activity via gene disruption is expected to attenuate JAK-STAT-mediated transcriptional programs, diminishing the expression of pro-survival and growth-promoting genes. This knockout model thus allows researchers to dissect the specific contributions of JAK2 to ovarian cancer pathobiology and to evaluate the dependence of these tumor cells on cytokine-driven signaling circuits.
This polyclonal JAK2 knockout cell product is suited for a wide array of applications, including investigation of JAK-STAT signaling dynamics in ovarian cancer, screening of JAK2-targeted small molecules, and mechanistic studies of chemoresistance. Researchers can employ Western blotting for JAK2 and phospho-STAT3, RT-qPCR for JAK2 mRNA quantification, proliferation assays (MTS/XTT), apoptosis detection by Annexin V/PI flow cytometry, and phospho-kinase antibody arrays to monitor pathway alterations. Functional assays such as cytokine stimulation, co-immunoprecipitation of receptor complexes, and migration/invasion analyses further enable detailed phenotypic characterization. For additional information or custom requests, please contact Ascent Research.
