The EFEMP1 Knockout AGS Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line, in which the EFEMP1 gene has been disrupted. This product provides a heterogeneous pool of cells with loss-of-function mutations in EFEMP1, enabling robust functional studies without clonal selection. The polyclonal format captures diverse mutational events, reducing the risk of clonal artifacts and offering a physiologically relevant model for dissecting the role of fibulin-3 in gastric cancer biology.
The AGS cell line is a widely used model of human gastric adenocarcinoma, originally established from a primary gastric cancer. These cells exhibit epithelial morphology and retain key characteristics of gastric cancer, including dysregulated growth factor signaling and invasive potential. AGS cells serve as a valuable platform for studying tumor cell behavior, drug responses, and the tumor microenvironment, making them an ideal host for targeted gene knockout experiments aimed at understanding gastric cancer pathogenesis.
EFEMP1 encodes fibulin-3, an extracellular matrix glycoprotein that participates in cell adhesion, migration, and modulation of growth factor signaling. Fibulin-3 interacts with integrins such as ITGB1 and ITGAV, and with matrix components including fibronectin and collagen, thereby bridging the ECM to intracellular signaling cascades. It is regulated by upstream factors TGFB1, EGF, and hypoxia, and its downstream effects involve ITGB1, AKT1, and matrix metalloproteinases MMP2 and MMP9. Consequently, EFEMP1 integrates signals from the ECM-receptor interaction, PI3K-Akt, TGF-beta, and focal adhesion pathways, with key nodes including EGFR, PI3K, AKT, mTOR, FAK, and SRC. Disruption of EFEMP1 thus perturbs these interconnected networks, affecting cellular responses to adhesive and soluble cues.
In the context of AGS gastric cancer cells, knockout of EFEMP1 likely alters the balance of pro- and anti-tumorigenic signals. Loss of fibulin-3 may impair cell adhesion and enhance migratory and invasive phenotypes, while also modulating AKT-dependent survival and proliferation pathways. This model is particularly relevant for studying the dual role of ECM proteins in tumor suppression and progression, and for evaluating how fibulin-3 deficiency influences gastric cancer cell behavior in response to chemotherapeutic agents or targeted therapies.
The EFEMP1 Knockout AGS Polyclonal Cells are suitable for a wide range of research applications, including gastric cancer biology, tumor microenvironment studies, and investigations into cell migration and drug resistance. Researchers can employ standard assays such as Western blotting, RT-qPCR, scratch wound migration, Transwell invasion, MTT proliferation, immunofluorescence, and co-immunoprecipitation to characterize the functional consequences of EFEMP1 loss. Additionally, phospho-AKT analysis can directly probe PI3K-Akt pathway activity. By leveraging this polyclonal knockout model, scientists can gain deeper insights into how fibulin-3 shapes gastric cancer progression and identify novel therapeutic targets. For further technical details or ordering information, please contact Ascent Research.
