The IGSF8 Knockout NCI-H1703 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the NCI-H1703 human lung squamous cell carcinoma line. This product features targeted disruption of the immunoglobulin superfamily member 8 (IGSF8) gene, providing a loss-of-function model to study the tumor-suppressive roles of IGSF8 in non-small cell lung cancer (NSCLC).
NCI-H1703 is a neoplastic lung epithelial cell line established from a primary squamous cell carcinoma and is widely employed as an in vitro model for NSCLC. It retains key characteristics of the tumor microenvironment, making it suitable for investigating molecular mechanisms underlying lung cancer progression and metastasis.
IGSF8, also designated CD316 or EWI-2, is an immunoglobulin superfamily member that functions as a negative regulator of cell motility and metastasis. It organizes tetraspanin-enriched microdomains by interacting directly with CD9, CD81, CD151, and integrin ??3??1. Through these complexes, IGSF8 suppresses PI3K/AKT phosphorylation, leading to reduced focal adhesion kinase (FAK) and Rho GTPase activity, which are essential for cell migration and invasion. Additionally, IGSF8 downregulates matrix metalloproteinase (MMP) expression, further limiting extracellular matrix degradation. Its expression is epigenetically silenced during epithelial-mesenchymal transition (EMT) by transcriptional repressors, linking IGSF8 loss to enhanced metastatic potential. Thus, knockout of IGSF8 disrupts this inhibitory network, de-repressing integrin-mediated adhesion signaling and actin cytoskeleton dynamics.
In the NCI-H1703 background, IGSF8 deletion is predicted to activate PI3K/AKT signaling, promote cell migration, and enhance invasive capacity. This polyclonal knockout model enables detailed dissection of the tetraspanin web and integrin interactions that restrain lung cancer cell motility. Given that low IGSF8 expression correlates with poor prognosis in lung adenocarcinoma, this tool is valuable for exploring the mechanistic underpinnings of metastasis and testing therapeutic interventions targeting downstream effectors such as FAK or AKT.
Researchers can utilize these polyclonal knockout cells in a range of functional assays, including wound healing and transwell invasion to quantify migration and invasion, cell adhesion assays to evaluate integrin-mediated attachment, and western blot analysis of phospho-AKT to assess signaling changes. Co-immunoprecipitation and immunofluorescence can further probe IGSF8-containing complexes and their localization. These cells are also suitable for drug sensitivity screens to identify compounds that selectively target IGSF8-deficient NSCLC. For additional information or technical support, please contact Ascent Research.
