The IGFBP5 Knockout NCI-H1703 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the human IGFBP5 gene. This loss-of-function model enables investigation of insulin-like growth factor binding protein 5 in a lung squamous cell carcinoma background. The polyclonal pool retains cellular heterogeneity, suitable for population-level functional studies, and is supplied ready-to-use for in vitro experimental workflows.
The NCI-H1703 host cell line is a human lung squamous cell carcinoma epithelial cell line derived from a patient with non-small cell lung cancer (NSCLC). These adherent cells provide a clinically relevant model for squamous cell carcinoma, a major NSCLC subtype, exhibiting growth factor dependence and invasive potential, making them ideal for studying tumor suppressor genes like IGFBP5.
At the molecular level, IGFBP5 binds IGF-I and IGF-II with high affinity, sequestering them to limit interaction with IGF1R and thereby suppress PI3K/AKT and MAPK/ERK signaling. Reduced IGF1R activation attenuates phosphorylation of AKT1 and ERK (MAPK3), diminishing activity of downstream effectors MTOR and FOXO3. IGFBP5 also interacts with LRP1 and integrin beta1, and its expression is regulated by TGFB1, CEBPD, and glucocorticoids. Downstream, IGFBP5 influences MMP2 and BAX expression, integrating control of proliferation, survival, and migration. By limiting IGF signaling, IGFBP5 suppresses cell cycle progression and enhances apoptotic sensitivity, reinforcing its tumor-suppressive capacity.
In NCI-H1703 cells, IGFBP5 is thought to act as a tumor suppressor. CRISPR/Cas9-mediated knockout allows assessment of IGFBP5 loss on oncogenic signaling and behavior in squamous cell carcinoma. This model is suited for dissecting IGF-driven growth and motility alterations, as lung squamous carcinomas often display dysregulated IGF signaling, and for exploring compensatory mechanisms when IGFBP5-mediated restraint of PI3K/AKT and MAPK pathways is abrogated.
Applications include functional genomics of tumor suppression in NSCLC, IGF signaling dissection, and therapeutic target evaluation. Readouts include proliferation (MTS), migration (Transwell), apoptosis (flow cytometry), phospho-signaling profiling of AKT/ERK, Western blotting, RT-qPCR, and colony formation assays. These polyclonal knockout cells support drug discovery programs targeting the IGF axis and basic cancer research. For more information, please contact Ascent Research.
