EFNB1 Knockout NCI-H1299 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the EFNB1 gene has been disrupted in the NCI-H1299 non-small cell lung carcinoma cell line. This polyclonal knockout model provides a genetically heterogeneous loss-of-function system for studying the role of ephrin-B1, a membrane-bound ligand of the Eph receptor tyrosine kinase family, in cancer cell biology.
NCI-H1299 cells are epithelial cells derived from a lymph node metastasis of a lung adenocarcinoma from a 43-year-old male. This cell line is widely employed as a model for non-small cell lung cancer, particularly in investigations of tumor cell migration, invasion, and metastasis, due to its well-characterized growth and signaling properties.
EFNB1 encodes ephrin-B1, which engages in bidirectional signaling upon binding to Eph receptors such as EphB1, EphB2, EphB3, and EphA4. Ephrin-B1 reverse signaling is regulated by upstream factors including WNT3A, TGFB1, and HOXA5, and it transduces signals through downstream effectors like SRC kinase, FAK, MAPK/ERK, and Rho GTPases (RhoA, Rac1). Adaptor proteins GRB4, Nck2, and PICK1 interact with ephrin-B1 to modulate downstream complexes.
In NCI-H1299 cells, disruption of EFNB1 is expected to impair ephrin-B1-mediated cell-cell repulsion and adhesion, thereby altering MAPK/ERK and Rho GTPase signaling pathways that govern cell migration and invasion. This knockout model thus offers a relevant tool for dissecting ephrin-B1-dependent mechanisms in lung cancer metastasis and for exploring crosstalk between Eph/ephrin signaling and other oncogenic pathways.
Typical research applications include wound healing assays, transwell migration and invasion assays, western blotting for ERK phosphorylation, immunofluorescence to assess Eph receptor activation, and RT-qPCR for EFNB1 expression levels. These polyclonal knockout cells are suited for studying ephrin-B1 function in non-small cell lung cancer, validating drug targets, and investigating the molecular underpinnings of metastatic progression. For further technical details or ordering information, please contact Ascent Research.
