The IGSF8 Knockout T-47D Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human T-47D breast ductal carcinoma cell line, featuring targeted disruption of the IGSF8 gene. This polyclonal knockout model provides a heterogeneous pool of cells with disrupted IGSF8 expression, enabling studies of gene function in a population context without clonal selection. The targeted disruption interferes with the production of functional IGSF8 protein, a transmembrane adhesion molecule that associates with tetraspanin partners to modulate cell surface signaling platforms.
The parental T-47D cell line is a widely used estrogen receptor-positive (ER+) and progesterone receptor-positive (PR+) human breast carcinoma model originally established from a pleural effusion of a ductal carcinoma patient. These cells retain hormone responsiveness and are frequently employed to investigate estrogen-dependent signaling pathways and endocrine therapy responses in breast cancer research. Their well-characterized genetic and phenotypic background makes T-47D a suitable host for studying genes involved in hormone-sensitive tumor progression.
IGSF8 (immunoglobulin superfamily member 8) is a transmembrane adhesion molecule that forms complexes with the tetraspanins CD81 and CD9 and binds integrins ??3??1 and ??5??1. These interactions organize tetraspanin-enriched microdomains that regulate integrin-mediated adhesion, migration, and intracellular signaling. IGSF8 modulates focal adhesion kinase (FAK) and ERK1/2 phosphorylation, as well as the PI3K/AKT pathway, often downstream of EGF/EGFR and estrogen cues. It also influences Rho GTPase activity and the matrix metalloproteinases MMP-2 and MMP-9, linking it to cytoskeletal remodeling and invasion. Association with ERM proteins (ezrin, radixin, moesin) ties IGSF8 to actin dynamics, establishing it as a key integrator of adhesion-dependent signal transduction.
In T-47D breast cancer cells, loss of IGSF8 is anticipated to disrupt tetraspanin?Cintegrin complexes, impairing adhesion and attenuating FAK and ERK1/2 phosphorylation. The hormone-responsive nature of T-47D cells makes this knockout model particularly suited for investigating crosstalk between estrogen receptor signaling and IGSF8-mediated pathways. By abolishing IGSF8, researchers can dissect its contribution to estrogen-driven proliferation, migration, and invasive potential, as well as its role in maintaining epithelial integrity. This polyclonal knockout population thus provides a physiologically relevant backdrop for studying breast cancer progression and metastasis.
Researchers can use these polyclonal knockout cells in Transwell migration and invasion assays, cell adhesion experiments, and co-immunoprecipitation studies to assess tetraspanin complex composition. Western blotting for phospho-FAK and phospho-ERK1/2, along with flow cytometry for integrin surface expression, enables monitoring of signaling outputs. RT-qPCR analysis of IGSF8 and downstream transcripts complements the functional readouts. Additionally, the cells serve as a model for hepatitis C virus entry studies, where IGSF8?CCD81 interactions are essential. For more information, please contact Ascent Research.
