EFHD1 Knockout NCI-H1299 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the NCI-H1299 NSCLC cell line with disrupted EFHD1 gene. This mixed population avoids clonal bias and provides a robust model for studying EFHD1’s role in cancer biology. The cells are supplied as a viable culture for immediate experimental use.
The parental NCI-H1299 cell line originates from a lymph node metastasis of a lung adenocarcinoma. It features p53 deficiency (biallelic TP53 deletion), while harboring wild-type KRAS and EGFR, making it a relevant model for p53-independent lung cancer mechanisms and metastasis research.
EFHD1 is a calcium-binding adaptor protein that orchestrates actin cytoskeleton dynamics, cell migration, and apoptosis. It interacts directly with F-actin, filamin A, myosin II, and calmodulin, positioning it to transduce calcium and inflammatory cues such as TNF-??/NF-??B signaling. Upon activation, EFHD1 couples to integrin ??1?CFAK?CSrc complexes, triggering Rac1 and RhoA GTPase cascades that regulate cofilin and LIMK, thereby driving actin polymerization and focal adhesion turnover. Concurrently, EFHD1 modulates MMP expression and caspase-3 activity, linking cytoskeletal rearrangements to invasion and cell death. Disruption of EFHD1 thus abolishes calcium-mediated remodeling, impairing migration and invasion.
In NCI-H1299 cells, EFHD1 knockout creates a functional deficiency in pathways essential for metastatic dissemination. As the parental line is derived from a lymph node metastasis and retains invasive properties, loss of EFHD1 substantially impairs cell motility, ECM invasion, and likely three-dimensional growth. This model allows dissection of calcium-dependent signaling nodes that drive lung adenocarcinoma progression independently of p53, offering a platform to evaluate anti-metastatic compounds targeting actin remodeling and integrin signaling.
Researchers can employ these cells for a range of assays, including wound healing and transwell invasion to measure migration/invasion, phalloidin staining and immunofluorescence for F-actin visualization, and phospho-kinase arrays for signaling network analysis. RNA-seq and western blotting reveal transcriptional and proteomic alterations, while flow cytometry (e.g., Annexin V/PI) detects apoptosis modulation. Ideal for functional genomics, drug screens targeting metastasis, and calcium signaling studies in lung cancer. For further information, contact Ascent Research.
