This product is a CRISPR/Cas9-edited polyclonal knockout cell population featuring targeted disruption of IGSF8 in the human LoVo colorectal adenocarcinoma cell line. The polyclonal format provides a heterogeneous pool of gene-edited cells, enabling functional studies without clonal selection artifacts. These cells serve as a robust loss-of-function model for dissecting IGSF8-dependent mechanisms in colorectal cancer.
LoVo cells, derived from a metastatic lymph node of a colorectal adenocarcinoma patient, are an established epithelial model for studying metastasis. They retain key colorectal cancer features, including relevant signaling pathway activity and marker expression, supporting reproducible experiments in oncology research.
IGSF8 (EWI-2) is a cell surface protein that resides in tetraspanin-enriched microdomains (TEMs) and interacts with tetraspanins CD9, CD81, and integrins ??3??1 and ??6??1. It regulates cell adhesion, migration, and proliferation. IGSF8 expression is governed by TGF-?? signaling and transcription factors SNAI1 and SP1. Its knockout disrupts downstream effectors such as FAK, ERK1/2, AKT, and the cell cycle regulators p21 and p27, thereby impairing integrin-mediated signaling and the PI3K/AKT and ERK pathways, which are frequently hyperactive in colorectal cancer.
In the LoVo colorectal adenocarcinoma context, IGSF8 knockout likely destabilizes tetraspanin webs, attenuating adhesion and pro-migratory signals. As IGSF8 contributes to metastasis in colorectal and other cancers, this model is valuable for studying its role in tumor invasiveness and proliferation and for examining how loss of IGSF8 reorganizes TEM-associated complexes and oncogenic signaling.
Applications include Transwell migration and invasion assays to measure metastatic potential, MTT or BrdU proliferation assays, and western blotting for phospho-AKT and phospho-ERK. Co-immunoprecipitation can assess tetraspanin complex integrity, while drug sensitivity assays with chemotherapeutics may uncover IGSF8-dependent vulnerabilities. For additional information, please contact Ascent Research.
