This product consists of a polyclonal population of NCI-H1703 lung adenocarcinoma epithelial cells in which the JAG2 gene has been disrupted via CRISPR/Cas9 genome editing. The resulting cell pool provides a genetically heterogeneous knockout model that retains the polyclonal nature of the parental line while enabling loss-of-function studies of the JAG2 ligand. As a polyclonal knockout product, it is suitable for functional assays where complete gene ablation at the population level is desired without requiring isolation of single-cell clones.
The NCI-H1703 cell line was originally derived from a primary lung adenocarcinoma of a 54-year-old male smoker and serves as a well-characterized model for non-small cell lung cancer. These cells exhibit epithelial morphology and are widely utilized to investigate tumor invasion, metastasis, and drug resistance mechanisms. The tumorigenic and invasive properties of NCI-H1703 cells make them particularly relevant for studying the molecular drivers of aggressive lung adenocarcinoma.
JAG2 is a canonical Notch ligand that directs cell fate, angiogenesis, and tumor progression. Upon binding NOTCH1-3 receptors on neighboring cells, it triggers ADAM17- and ??-secretase-mediated cleavage, releasing NICD. NICD translocates to the nucleus, forming a complex with RBPJ and MAML1 that activates target genes HES1, HEY1, MYC, and CCND1. Upstream regulators TGFB1, HIF1A, and ATOH1 modulate this pathway, and NICD itself participates in feedback regulation. The JAG2-NOTCH axis thus links extracellular signals to transcriptional programs controlling proliferation, survival, and epithelial-mesenchymal transition.
In the NCI-H1703 background, loss of JAG2 likely disrupts autocrine and paracrine Notch signaling that contributes to invasive and metastatic phenotypes. JAG2-driven NICD activation enhances HES1 and HEY1 expression, promoting epithelial-mesenchymal transition and cancer stem cell traits; therefore, knockout provides a means to study ligand-mediated Notch activation in tumor progression. Additionally, this model permits dissection of cross-talk with TGF-?? and Wnt pathways commonly co-opted in lung cancer.
Researchers can employ this polyclonal JAG2 knockout cell pool in Notch signaling studies, invasion and metastasis assays, and drug resistance profiling. Representative techniques include western blotting for JAG2 and HES1, RT-qPCR for HES1/HEY1, transwell migration/invasion assays, flow cytometric analysis of NOTCH receptor expression, and co-immunoprecipitation for JAG2-NOTCH interactions. RNA-seq can map global changes in Notch target gene expression. The model is also applicable to angiogenesis and developmental biology research. For further technical details, please contact Ascent Research.
