The DYNLT3 Knockout NCI-H1299 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population designed for loss-of-function studies of the human DYNLT3 gene. Generated in the NCI-H1299 non-small cell lung carcinoma line, this polyclonal knockout model captures heterogeneous gene disruption, enabling robust phenotypic analysis without the bottleneck of clonal selection.
NCI-H1299 is a human non-small cell lung carcinoma epithelial line derived from lymph node metastasis. Characterized by p53 deficiency and wild-type KRAS, these cells serve as a key model for investigating proliferation, apoptosis, migration, and drug sensitivity in lung cancer. Their metastatic origin makes them particularly suitable for studying motility and invasion.
DYNLT3 encodes a light chain of the cytoplasmic dynein motor complex that facilitates minus-end-directed microtubule transport. FOXM1 transcriptionally activates DYNLT3, while CDK1 and Aurora A kinases phosphorylate the protein. Within the dynein complex, DYNLT3 interacts with dynein intermediate chain (DYNC1I1) and heavy chain (DYNC1H1). Functionally, DYNLT3 overexpression enhances AKT phosphorylation, upregulates Cyclin B1, and strengthens integrin-mediated adhesion, thereby promoting cell cycle progression and migration??a FOXM1?CDYNLT3?CAKT signaling axis implicated in tumor aggressiveness.
In the p53-deficient NCI-H1299 context, DYNLT3 knockout allows dissection of dynein-dependent pathways that sustain NSCLC cell survival and metastasis. Researchers can interrogate how loss of this light chain alters AKT signaling, microtubule organization, and invasive behavior, leveraging the cell line??s inherent metastatic phenotype to reveal mechanisms of lung cancer progression.
Applications include biochemical dissection of the FOXM1?CDYNLT3?CAKT cascade via western blot (DYNLT3, AKT, phospho-AKT) and RT-qPCR, as well as co-immunoprecipitation to assess dynein complex integrity. Immunofluorescence co-localization with microtubules and functional assays like MTT proliferation and Transwell migration/invasion provide integrated readouts. This polyclonal population is also amenable to dynein inhibitor screening. For inquiries, contact Ascent Research.
