The IGSF8 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human esophageal squamous cell carcinoma line KYSE-150. This loss-of-function model eliminates IGSF8 protein expression through heterogeneous gene disruption across the cell pool, avoiding clonal selection artifacts. The polyclonal format enables population-level functional studies of cell adhesion, migration, and signaling in a cancer-relevant background.
KYSE-150 is a poorly differentiated esophageal squamous cell carcinoma cell line that retains aggressive features such as high migratory potential and anchorage-independent growth. It provides a clinically relevant host for examining genes involved in tumor progression and metastasis, and its genetic background makes it suitable for functional genomics and oncogenic signaling studies.
IGSF8 (EWI-2) is a tetraspanin-enriched microdomain component that directly interacts with CD9 and CD81 and associates with integrins ??3??1 and ??6??1. It regulates integrin-mediated signaling, influencing FAK, Src, PI3K/AKT, and MAPK/ERK pathways, and modulates Rho GTPases RhoA and Rac1 to control cytoskeletal dynamics and cell migration. Disruption of IGSF8 alters matrix metalloproteinase expression and cell cycle regulation, highlighting its central role in adhesion-dependent signaling networks.
In KYSE-150 cells, IGSF8 knockout disrupts the balance of adhesion and motility, potentially impairing invasive behavior and altering oncogenic pathway activation. The polyclonal population allows assessment of heterogeneous responses to IGSF8 loss, mimicking tumor heterogeneity, and is invaluable for studying ESCC metastasis mechanisms and context-dependent tumor suppressor functions.
Typical applications include transwell migration/invasion assays, cell adhesion measurements, proliferation analyses, Western blotting for phospho-FAK, AKT, and ERK1/2, and immunofluorescence/flow cytometry for tetraspanin complex visualization. These cells can also support drug sensitivity screens targeting PI3K and MAPK pathways, and co-culture experiments with stromal cells. For more information, contact Ascent Research.
