IGSF8 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disruption of the IGSF8 gene in the HCT 116 human colorectal carcinoma background. This heterogeneous pool of gene-edited cells provides a loss-of-function model for studying IGSF8 function in cell adhesion, migration, and tetraspanin microdomain organization, avoiding clonal isolation artifacts.
The HCT 116 cell line, a widely used colorectal adenocarcinoma model, originates from a male patient and features MSI-H, KRAS G13D, ??-catenin, and MLH1-deficiency. These mutations drive constitutive Wnt and MAPK activation, making it an ideal platform for investigating epithelial tumor biology, metastasis, and integrin-mediated signaling.
IGSF8 (immunoglobulin superfamily member 8, also known as CD316) belongs to the tetraspanin family and serves as a key organizer of tetraspanin-enriched microdomains (TEMs). It forms complexes with partner tetraspanins CD9 and CD81, and integrins ??3??1 and ??6??1, linking the extracellular matrix to intracellular signaling. Upon engagement of fibronectin, these complexes activate the PI3K/AKT pathway, leading to phosphorylation of downstream effectors including FAK and paxillin, and modulating Rho GTPase activity to drive cytoskeletal reorganization and cell migration. IGSF8 function is further regulated by EGF receptor signaling and other tetraspanins such as CD82 and CD151. CRISPR/Cas9-mediated disruption of IGSF8 disrupts TEM assembly, resulting in diminished integrin-mediated adhesion, reduced PI3K/AKT signaling, and impaired migratory capacity.
In the HCT 116 background, constitutive KRAS and ??-catenin mutations drive oncogenic signaling independently of IGSF8, providing a unique opportunity to dissect tetraspanin-specific contributions to cell adhesion and migration. IGSF8 knockout in this context reveals how integrin-mediated PI3K/AKT activation governs metastatic potential, and enables investigation of its role in immune evasion and viral susceptibility.
This polyclonal knockout population is optimized for functional assays including Transwell migration, cell adhesion to fibronectin, and phospho-AKT analysis to quantify signaling output. Co-immunoprecipitation and mass spectrometry can map altered interactomes, while flow cytometry and immunofluorescence enable profiling of surface integrins and TEM organization. The model supports research on colorectal cancer metastasis, tetraspanin biology, integrin signaling, immune checkpoint regulation, and drug target validation. For additional technical details, please contact Ascent Research.
