The IGSF8 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human HT29 colorectal adenocarcinoma cell line. This product features a heterogeneous loss-of-function model achieved by CRISPR-mediated gene disruption, without single-cell clonal isolation. The pooled knockout cells maintain genetic diversity, facilitating robust functional studies of IGSF8 in a population context, suitable for perturbation of IGSF8-dependent processes while preserving the cellular heterogeneity inherent to polyclonal cultures.
HT29 is a well-characterized human colorectal adenocarcinoma cell line with epithelial morphology, commonly employed to investigate colon cancer biology. Bearing mutations in APC and TP53, HT29 cells provide a relevant model for studying tumor cell adhesion, migration, and invasion. Their epithelial nature supports analysis of cell?Ccell and cell?Cmatrix interactions, making them an ideal host for examining the role of adhesion molecules such as IGSF8 in a colorectal cancer context.
IGSF8 (EWI-2) is a transmembrane immunoglobulin superfamily protein that operates within tetraspanin-enriched microdomains. It directly interacts with tetraspanins CD9 and CD81 and associates with integrins ??3??1 and ??6??1 to regulate cell adhesion, migration, and proliferation. These interactions drive downstream activation of FAK and Src kinases, leading to cytoskeletal reorganization. Upstream, IGSF8 function is influenced by cytokine receptors and other tetraspanin web components. Through this network, IGSF8 integrates extracellular signals to modulate crucial cellular behaviors, and its knockout disrupts these adhesion-dependent signaling cascades.
In HT29 colorectal adenocarcinoma cells, loss of IGSF8 is predicted to disrupt the tetraspanin-integrin axis essential for tumor cell motility and metastatic potential. Since HT29 constitutively expresses CD9, CD81, and relevant integrins, the polyclonal knockout population enables dissection of IGSF8-dependent adhesion and migration pathways in colon cancer. This model is particularly valuable for examining mechanisms of colorectal cancer metastasis and for assessing the reliance of HT29 cells on tetraspanin-mediated signaling for invasive phenotypes.
These polyclonal knockout cells are intended for diverse research applications, including cell adhesion and migration studies using Transwell and adhesion assays, analysis of tetraspanin web interactions via co-immunoprecipitation and immunofluorescence, and drug response screening targeting the integrin-FAK-Src pathway. Knockout validation and functional characterization can be performed by Western blotting, RT-qPCR, and flow cytometry, while phospho-FAK and phospho-Src analyses provide direct signaling readouts. For more information or to discuss custom requirements, please contact Ascent Research.
