The IGFBP5 Knockout NCI-H1299 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population targeting the IGFBP5 gene in the NCI-H1299 cell line. This heterogeneous knockout pool provides a robust loss-of-function model for studying IGFBP5 without clonal selection bias. The polyclonal format preserves genetic diversity, minimizing artifacts and offering a physiologically relevant system for functional analyses. As a gene-disrupted cell population, it is suited for comparative studies with wild-type controls in cancer biology and signal transduction research.
NCI-H1299 is a human non-small cell lung carcinoma cell line derived from a metastatic lymph node. It exhibits epithelial morphology, lacks functional p53, and displays high tumorigenic and metastatic potential in vivo. This background makes it an ideal host for investigating molecular drivers of lung cancer metastasis and drug resistance. The well-characterized behavior of NCI-H1299 cells in migration, invasion, and proliferation assays ensures reproducible experimental outcomes.
IGFBP5 encodes insulin-like growth factor binding protein 5, a key regulator of IGF bioavailability and signaling. It binds IGF1 and IGF2, modulating IGF1R activation and downstream PI3K/AKT and MAPK/ERK pathways. IGFBP5 also interacts with fibronectin and heparin, influencing cell adhesion and matrix remodeling. Its expression is regulated by p53, TGF-beta, and retinoic acid. Knockout of IGFBP5 abolishes its IGF-sequestering function and alters phosphorylation of AKT and ERK1/2, impacting cell survival, proliferation, and migration.
In NCI-H1299 cells, IGFBP5 deletion removes a protein with context-dependent roles in tumor progression. This model enables dissection of IGFBP5??s contributions to metastatic behaviors such as invasion, anoikis resistance, and extracellular matrix remodeling. The polyclonal knockout pool mimics tumor heterogeneity, facilitating studies on IGF-1 receptor signaling crosstalk with AKT/mTOR and ERK pathways. It is a valuable tool for exploring mechanisms of drug resistance in non-small cell lung cancer.
Typical applications include lung cancer biology, metastasis investigation, and IGF signaling studies. The knockout cells are suitable for functional assays such as transwell migration and invasion, soft agar colony formation, and cell viability assessments. Western blotting and RT-qPCR are employed to validate target protein knockdown and assess downstream effectors like phospho-AKT. Co-immunoprecipitation can probe altered protein interactions. This model supports drug resistance screening and functional genomics. For further information, contact Ascent Research.
