CRISPR/Cas9-edited polyclonal knockout cell population for JAG2 gene disruption in human HCT 116 colorectal carcinoma cells. This product provides a pool of gene-disrupted cells, facilitating loss-of-function studies without clonal isolation.
HCT 116 is a widely used epithelial cell line derived from colorectal carcinoma, harboring a KRAS G13D mutation. It serves as a robust model for cancer biology, drug screening, and signal transduction research.
JAG2 encodes a transmembrane ligand for Notch receptors (NOTCH1-4). Upon cell-cell contact, JAG2 activates Notch signaling, leading to gamma-secretase cleavage and release of the NICD, which translocates to the nucleus and forms complexes with RBPJ and MAML1 to drive expression of target genes such as HES1, HEY1, MYC, and CCND1. JAG2 function is modulated by upstream factors including MYC, NF-??B, hypoxia-inducible factors, and Wnt signaling, while its activity is regulated by interacting proteins such as MIB1 and ADAM17. Knockout of JAG2 disrupts this cascade, attenuating Notch-dependent transcription and downstream cellular responses.
In the HCT 116 colorectal cancer context, JAG2 knockout impairs Notch-driven proliferation, survival, and migration, and may affect epithelial-to-mesenchymal transition. This disruption is particularly relevant given the frequent dysregulation of Notch signaling in colorectal carcinoma and its association with poor prognosis. The polyclonal knockout population enables interrogation of JAG2’s role in tumor cell behavior without clonal selection bias.
These knockout cells are suitable for functional studies of the Notch pathway, including analysis of proliferation (CCK-8, BrdU), migration and invasion (Transwell assays), and apoptosis (Annexin V staining). They support drug screening for Notch inhibitors (e.g., gamma-secretase inhibitors) and assessment of pathway activation via western blotting for NICD and HES1, RT-qPCR for HES1, HEY1, MYC, and flow cytometry for surface Notch1. RNA-seq and other omics approaches can be used to map JAG2-dependent transcriptional landscapes. For further details, please contact Ascent Research.
